TY - JOUR
AU - Radák, Zsolt
AU - Torma, Ferenc Gergely
AU - Berkes, István
AU - Goto, Sataro
AU - Mimura, Tatsuya
AU - Pósa, Anikó
AU - Balogh, László
AU - Boldogh, Istvan
AU - Suzuki, Katsuhiko
AU - Higuchi, Mitsuru
AU - Koltai, Erika
TI - Exercise effects on physiological function during aging
JF - FREE RADICAL BIOLOGY AND MEDICINE
J2 - FREE RADICAL BIO MED
VL - 132
ET - 0
PY - 2019
SP - 33
EP - 41
PG - 9
SN - 0891-5849
DO - 10.1016/j.freeradbiomed.2018.10.444
UR - https://m2.mtmt.hu/api/publication/30319457
ID - 30319457
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Hao, W
AU - Qi, T
AU - Pan, L
AU - Wang, R
AU - Zhu, B
AU - Aguilera-Aguirre, L
AU - Radák, Zsolt
AU - Hazra, TK
AU - Vlahopoulos, SA
AU - Bácsi, Attila
AU - Brasier, AR
AU - Ba, X
AU - Boldogh, I
TI - Effects of the stimuli-dependent enrichment of 8-oxoguanine DNA glycosylase1 on chromatinized DNA.
JF - REDOX BIOLOGY
J2 - REDOX BIOL
VL - 18
PY - 2018
SP - 43
EP - 53
PG - 11
SN - 2213-2317
DO - 10.1016/j.redox.2018.06.002
UR - https://m2.mtmt.hu/api/publication/3390728
ID - 3390728
N1 - Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, TX 77555, United States
Internal Medicine, University of Texas Medical Branch at Galveston, Galveston, TX 77555, United States
Sealy Center for Molecular Medicine, University of Texas Medical Branch at Galveston, Galveston, TX 77555, United States
School of Life Science, Northeast Normal University, Changchun, China
Science Research Center of China-Japan Union Hospital, Jilin University, Changchun, China
Department of Physiology, Xiangya Medicine School in Central South University, Changsha, Hunan 410078, China
Research Institute of Sport Science, Semmelweis University, Budapest, Hungary
National and Kapodistrian University of Athens, Faculty of Medicine, Athens, Greece
Department of Immunology, Faculty of Medicine, University of Debrecen, Hungary
Cited By :30
Export Date: 19 October 2022
Correspondence Address: Boldogh, I.; Department of Microbiology and Immunology University of Texas Medical Branch at Galveston, 301 University Blvd, United States; email: sboldogh@utmb.edu
Chemicals/CAS: DNA, 9007-49-2; DNA glycosyltransferase, 70356-40-0; RNA, 63231-63-0; Chromatin; DNA; DNA Glycosylases; oxoguanine glycosylase 1, human; Reactive Oxygen Species; Tumor Necrosis Factor-alpha
AB - 8-Oxoguanine DNA glycosylase 1 (OGG1) initiates the base excision repair pathway by removing one of the most abundant DNA lesions, 8-oxo-7,8-dihydroguanine (8-oxoG). Recent data showed that 8-oxoG not only is a pro-mutagenic genomic base lesion, but also functions as an epigenetic mark and that consequently OGG1 acquire distinct roles in modulation of gene expression. In support, lack of functional OGG1 in Ogg1(-/-) mice led to an altered expression of genes including those responsible for the aberrant innate and adaptive immune responses and susceptibility to metabolic disorders. Therefore, the present study examined stimulus-driven OGG1-DNA interactions at whole genome level using chromatin immunoprecipitation (ChIP)-coupled sequencing, and the roles of OGG1 enriched on the genome were validated by molecular and system-level approaches. Results showed that signaling levels of cellular ROS generated by TNFalpha, induced enrichment of OGG1 at specific sites of chromatinized DNA, primarily in the regulatory regions of genes. OGG1-ChIP-ed genes are associated with important cellular and biological processes and OGG1 enrichment was limited to a time scale required for immediate cellular responses. Prevention of OGG1-DNA interactions by siRNA depletion led to modulation of NF-kappaB's DNA occupancy and differential expression of genes. Taken together these data show TNFalpha-ROS-driven enrichment of OGG1 at gene regulatory regions in the chromatinized DNA, which is a prerequisite to modulation of gene expression for prompt cellular responses to oxidant stress.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Yada, Koichi
AU - Suzuki, Katsuhiko
AU - Oginome, Natsumi
AU - Ma, Sihui
AU - Fukuda, Youichi
AU - Iida, Akira
AU - Radák, Zsolt
TI - Single Dose Administration of Taheebo Polyphenol Enhances Endurance Capacity in Mice
JF - SCIENTIFIC REPORTS
J2 - SCI REP
VL - 8
PY - 2018
IS - 1
SN - 2045-2322
DO - 10.1038/s41598-018-33029-2
UR - https://m2.mtmt.hu/api/publication/30338059
ID - 30338059
AB - Endurance capacity is important for maintenance of quality of life as well as performance of endurance athletes. In order to improve endurance, intake of nutritional supplements as well as exercise training is also important. Indeed, polyphenolic extracts from plants are known to improve endurance capacity via increase of fatty acid utilization, mitochondrial biogenesis or inhibition of oxidative stress. Taheebo, the extract obtained from inner bark of Tabebuia avellanedae has been reported to have beneficial effects for treatment of inflammation, oxidative stress and obesity. Here, we investigated the effects and mechanisms of polyphenol fraction of taheebo (taheebo polyphenol; TP) on endurance capacity of mice. Single dose administration of TP significantly increased running time until exhaustion. Acute TP administration increased blood glucose and muscle glycogen levels (p < 0.05) through alteration on expression level of genes involved with glycogen metabolism and gluconeogenesis. Furthermore, TP administration decreased exercise-induced increase of protein carbonyls in skeletal muscle. These results suggest that TP administration improve endurance capacity via up-regulation of skeletal muscle glycogen levels and maintenance of blood glucose by acceleration of gluconeogenesis as well as inhibition of exercise-induced oxidative stress. Single administration of TP also increased phosphorylation of AMP-activated protein kinase (AMPK) and gene expression level of sirtuin 1 (SIRT1) but did not change the marker of mitochondrial biogenesis.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Koltai, Erika
AU - Bori, Zoltán
AU - Chabert, C
AU - Dubouchaud, H
AU - Naito, H
AU - Machida, S
AU - Davies, KJ
AU - Murlasits, Zsolt
AU - Fry, AC
AU - Boldogh, I
AU - Radák, Zsolt
TI - SIRT1 may play a crucial role in overload-induced hypertrophy of skeletal muscle
JF - JOURNAL OF PHYSIOLOGY-LONDON
J2 - J PHYSIOL-LONDON
VL - 595
PY - 2017
IS - 11
SP - 3361
EP - 3376
PG - 16
SN - 0022-3751
DO - 10.1113/JP273774
UR - https://m2.mtmt.hu/api/publication/3202563
ID - 3202563
AB - Significant skeletal muscle mass guarantees functional wellbeing and is important for high level performance in many sports. Although the molecular mechanism for skeletal muscle hypertrophy has been well-studied, it still is not completely understood. In the present study, we used a functional overload model to induce plantaris muscle hypertrophy by surgically removing the soleus, and gastrocnemius muscles in rats. Two weeks of muscle ablation resulted in a 40% increase in muscle mass, which was associated with a significant increase in SIRT1 content and activity (P < 0.001). SIRT1-regulated Akt, eNOS, GLUT4 levels were also induced in hypertrophied muscles, and SIRT1 levels correlated with muscle mass, paired box protein 7 (Pax7), proliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt) levels. Alternatively, decreased FOXO1 and increased K48 polyubiquitination also suggest that SIRT1 could also be involved in the catabolic process of hypertrophy. Furthermore, increased levels of K63 and muscle RING finger 2 (MuRF2) protein could also be important enhancers of muscle mass. We report here that the levels of miR1 and miR133a decrease in hypertrophy and negatively correlate with muscle mass, SIRT1, and Nampt levels. Our results reveal a strong agreement between SIRT1 levels and activity, SIRT1 regulated pathways, and overload-induced hypertrophy. These findings, along with the well-known regulatory roles that SIRT1 plays in modulating both anabolic and catabolic pathways, allow us to propose the hypothesis that SIRT1 may actually play a crucial causal role in overload induced hypertrophy of skeletal muscle. This hypothesis will now require rigorous direct and functional testing. This article is protected by copyright. All rights reserved.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Suwa, M
AU - Nakano, H
AU - Radák, Zsolt
AU - Kumagai, S
TI - Effects of nitric oxide synthase inhibition on fiber-type composition, mitochondrial biogenesis, and SIRT1 expression in rat skeletal muscle
JF - JOURNAL OF SPORTS SCIENCE AND MEDICINE
J2 - J SPORT SCI MED
VL - 14
PY - 2015
IS - 3
SP - 548
EP - 555
PG - 8
SN - 1303-2968
UR - https://m2.mtmt.hu/api/publication/2990840
ID - 2990840
AB - It was hypothesized that nitric oxide synthases (NOS) regulated SIRT1 expression and lead to a corresponding changes of contractile and metabolic properties in skeletal muscle. The purpose of the present study was to investigate the influence of long-term inhibition of nitric oxide synthases (NOS) on the fiber-type composition, metabolic regulators such as and silent information regulator of transcription 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha), and components of mitochondrial biogenesis in the soleus and plantaris muscles of rats. Rats were assigned to two groups: control and NOS inhibitor (N (omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME), ingested for 8 weeks in drinking water)-treated groups. The percentage of Type I fibers in the L-NAME group was significantly lower than that in the control group, and the percentage of Type IIA fibers was concomitantly higher in soleus muscle. In plantaris muscle, muscle fiber composition was not altered by L-NAME treatment. L-NAME treatment decreased the cytochrome C protein expression and activity of mitochondrial oxidative enzymes in the plantaris muscle but not in soleus muscle. NOS inhibition reduced the SIRT1 protein expression level in both the soleus and plantaris muscles, whereas it did not affect the PGC-1alpha protein expression. L-NAME treatment also reduced the glucose transporter 4 protein expression in both muscles. These results suggest that NOS plays a role in maintaining SIRT1 protein expression, muscle fiber composition and components of mitochondrial biogenesis in skeletal muscle. Key pointsNOS inhibition by L-NAME treatment decreased the SIRT1 protein expression in skeletal muscle.NOS inhibition induced the Type I to Type IIA fiber type transformation in soleus muscle.NOS inhibition reduced the components of mitochondrial biogenesis and glucose metabolism in skeletal muscle.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Mosaferi Ziaaldini, Mohammad
AU - Koltai, Erika
AU - Csende, Zsolt
AU - Goto, Sataro
AU - Boldogh, Istvan
AU - Taylor, Albert W
AU - Radák, Zsolt
TI - Exercise training increases anabolic and attenuates catabolic and apoptotic processes in aged skeletal muscle of male rats
JF - EXPERIMENTAL GERONTOLOGY
J2 - EXP GERONTOL
VL - 67
PY - 2015
SP - 9
EP - 14
PG - 6
SN - 0531-5565
DO - 10.1016/j.exger.2015.04.008
UR - https://m2.mtmt.hu/api/publication/2883904
ID - 2883904
AB - Abstract Aging results in significant loss of mass and function of the skeletal muscle, which negatively impacts the quality of life. In this study we investigated whether aerobic exercise training has the potential to alter anabolic and catabolic pathways in the skeletal muscle. Five and twenty eight month old rats were used in the study. Aging resulted in decreased levels of follistatin/mTOR/Akt/Erk activation and increased myostatin/Murf1/2, proteasome subunits, and protein ubiquitination levels. In addition, TNF-α, reactive oxygen species (ROS), p53, and Bax levels were increased while Bcl-2 levels were decreased in the skeletal muscle of aged rats. Six weeks of exercise training at 60% of VO2max reversed the age-associated activation of catabolic and apoptotic pathways and increased anabolic signaling. The results suggest that the age-associated loss of muscle mass and cachexia could be due to the orchestrated down-regulation of anabolic and up-regulation of catabolic and pro-apoptotic processes. These metabolic changes can be attenuated by exercise training.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Hart, Nikolett
AU - Szűcs (Sárga), Linda
AU - Csende, Zsolt
AU - Koch, Lauren G
AU - Britton, Steven L
AU - Davies, Kelvin J A
AU - Radák, Zsolt
TI - Resveratrol attenuates exercise-induced adaptive responses in rats selectively bred for low running performance
JF - DOSE-RESPONSE
J2 - DOSE RESP
VL - 12
PY - 2014
IS - 1
SP - 57
EP - 71
PG - 15
SN - 1559-3258
DO - 10.2203/dose-response.13-010.Radak
UR - https://m2.mtmt.hu/api/publication/2597018
ID - 2597018
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Radák, Zsolt
AU - Ihász, Ferenc
AU - Koltai, Erika
AU - Goto, S
AU - Taylor, AW
AU - Boldogh, I
TI - The redox-associated adaptive response of brain to physical exercise
JF - FREE RADICAL RESEARCH
J2 - FREE RADIC RES
VL - 48
PY - 2014
IS - 1
SP - 84
EP - 92
PG - 9
SN - 1071-5762
DO - 10.3109/10715762.2013.826352
UR - https://m2.mtmt.hu/api/publication/2391402
ID - 2391402
N1 - Megjegyzés-23616436
Megjegyzés-23543214
FN: Thomson Reuters Web of Knowledge
Megjegyzés-23543397
FN: Thomson Reuters Web of Knowledge
Megjegyzés-23542217
FN: Thomson Reuters Web of Knowledge
AB - Abstract Reactive oxygen species (ROS) are continuously generated during metabolism. ROS are involved in redox signalling but, in significant concentrations they can greatly elevate oxidative damage leading to neurodegeneration. Because of the enhanced sensitivity of brain to ROS, it is especially important to maintain a normal redox state in brain and spinal cord cell types. The complex effects of exercise benefit brain function, including functional enhancement as well as preventive and therapeutic roles. Exercise can induce neurogenesis via neurotrophic factors, increase capillarization, decrease oxidative damage, and enhance repair of oxidative damage. Exercise is also effective in attenuating age-associated loss in brain function, which suggests that physical activity-related complex metabolic and redox changes are important for a healthy neural system.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Hart, Nikolett
AU - Szűcs (Sárga), Linda
AU - Csende, Zsolt
AU - Koltai, Erika
AU - Koch, LG
AU - Britton, SL
AU - Davies, KJA
AU - Kouretas, D
AU - Wessner, B
AU - Radák, Zsolt
TI - Resveratrol enhances exercise training responses in rats selectively bred for high running performance
JF - FOOD AND CHEMICAL TOXICOLOGY
J2 - FOOD CHEM TOXICOL
VL - 61
PY - 2013
SP - 53
EP - 59
PG - 7
SN - 0278-6915
DO - 10.1016/j.fct.2013.01.051
UR - https://m2.mtmt.hu/api/publication/2237194
ID - 2237194
N1 - Megjegyzés-23542230
N1 Funding Details: RO1 DK077200, NIH, National Institutes of Health
Megjegyzés-23543273
N1 Funding Details: RO1 DK077200, NIH, National Institutes of Health
Megjegyzés-23644230
N1 Funding Details: RO1 DK077200, NIH, National Institutes of Health
AB - High Capacity Runner (HCR) rats have been developed by divergent artificial selection for treadmill endurance running capacity to explore an aerobic biology-disease connection. The beneficial effects of resveratrol supplementation have been demonstrated in endurance running and the antioxidant capacity of resveratrol is also demonstrated. In this study we examine whether 12weeks of treadmill exercise training and/or resveratrol can enhance performance in HCR. Indeed, resveratrol increased aerobic performance and strength of upper limbs of these rats. Moreover, we have found that resveratrol activated the AMP-activated protein kinase, SIRT1, and mitochondrial transcription factor A (p<0.05). The changes in mitochondrial fission/fusion and Lon protease/HSP78 levels suggest that exercise training does not significantly induce damage of proteins. Moreover, neither exercise training nor resveratrol supplementation altered the content of protein carbonyls. Changes in the levels of forkhead transcription factor 1 and SIRT4 could suggest increased fat utilization and improved insulin sensitivity. These data indicate, that resveratrol supplementation enhances aerobic performance due to the activation of the AMPK-SIRT1-PGC-1alpha pathway.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Radák, Zsolt
AU - Koltai, Erika
AU - Taylor, AW
AU - Higuchi, M
AU - Kumagai, S
AU - Ohno, H
AU - Goto, S
AU - Boldogh, I
TI - Redox-regulating sirtuins in aging, caloric restriction, and exercise
JF - FREE RADICAL BIOLOGY AND MEDICINE
J2 - FREE RADICAL BIO MED
VL - 58
PY - 2013
SP - 87
EP - 97
PG - 11
SN - 0891-5849
DO - 10.1016/j.freeradbiomed.2013.01.004
UR - https://m2.mtmt.hu/api/publication/2270900
ID - 2270900
N1 - Megjegyzés-23123201
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric
oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-
36-0; sirtinol, 410536-97-9
Megjegyzés-23123334
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric
oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-
36-0; sirtinol, 410536-97-9
Megjegyzés-23123497
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric
oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-
36-0; sirtinol, 410536-97-9
Megjegyzés-23127588
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric
oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-
36-0; sirtinol, 410536-97-9
Megjegyzés-23127879
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-36-0; sirtinol, 410536-97-9
Megjegyzés-23128556
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric
oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-
36-0; sirtinol, 410536-97-9
Megjegyzés-23128604
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric
oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-
36-0; sirtinol, 410536-97-9
Megjegyzés-23130511
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-36-0; sirtinol, 410536-97-9
Megjegyzés-23130837
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric
oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-
36-0; sirtinol, 410536-97-9
Megjegyzés-23123224
N1 : Chemicals/CAS8 hydroxyguanine, 5614-64-2; deoxyribonuclease I, 9003-98-9; endothelial nitric
oxide synthase, 503473-02-7; nicotinamide phosphoribosyltransferase, 9030-27-7; resveratrol, 501-
36-0; sirtinol, 410536-97-9
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Szűcs (Sárga), Linda
AU - Hart, Nikolett
AU - Koch, L G
AU - Britton, S L
AU - Hajas, György
AU - Boldogh, I
AU - Ba, X
AU - Radák, Zsolt
TI - Aerobic endurance capacity affects spatial memory and SIRT1 is a potent modulator of 8-oxoguanine repair.
JF - NEUROSCIENCE
J2 - NEUROSCIENCE
VL - 252
PY - 2013
SP - 326
EP - 336
PG - 11
SN - 0306-4522
DO - 10.1016/j.neuroscience.2013.08.020
UR - https://m2.mtmt.hu/api/publication/2391403
ID - 2391403
N1 - Megjegyzés-23488843
N1 Funding Details: RO1 ES018948, NIEHS, National Institute of Environmental Health Sciences
N1 Funding Details: AI062885, NIAID, National Institute of Allergy and Infectious Diseases
N1 Funding Details: AG 021830, NIA, National Institute on Aging
Megjegyzés-23491334
N1 Funding Details: RO1 ES018948, NIEHS, National Institute of Environmental Health Sciences
N1 Funding Details: AI062885, NIAID, National Institute of Allergy and Infectious Diseases
N1 Funding Details: AG 021830, NIA, National Institute on Aging
Megjegyzés-23544532
N1 Funding Details: RO1 ES018948, NIEHS, National Institute of Environmental Health Sciences
N1 Funding Details: AI062885, NIAID, National Institute of Allergy and Infectious Diseases
N1 Funding Details: AG 021830, NIA, National Institute on Aging
Megjegyzés-23623112
N1 Funding Details: RO1 ES018948, NIEHS, National Institute of Environmental Health Sciences
N1 Funding Details: AI062885, NIAID, National Institute of Allergy and Infectious Diseases
N1 Funding Details: AG 021830, NIA, National Institute on Aging
Megjegyzés-23642704
N1 Funding Details: RO1 ES018948, NIEHS, National Institute of Environmental Health Sciences
N1 Funding Details: AI062885, NIAID, National Institute of Allergy and Infectious Diseases
N1 Funding Details: AG 021830, NIA, National Institute on Aging
Megjegyzés-23644598
N1 Funding Details: RO1 ES018948, NIEHS, National Institute of Environmental Health Sciences
N1 Funding Details: AI062885, NIAID, National Institute of Allergy and Infectious Diseases
N1 Funding Details: AG 021830, NIA, National Institute on Aging
AB - Regular exercise promotes brain function via a wide range of adaptive responses, including the increased expression of antioxidant and oxidative DNA damage-repairing systems. Accumulation of oxidized DNA base lesions and strand breaks is etiologically linked to for example aging processes and age-associated diseases. Here we tested whether exercise training has an impact on brain function, extent of neurogenesis, and expression of 8-oxoguanine DNA glycosylase-1 (Ogg1) and SIRT1 (silent mating type information regulation 2 homolog). To do so, we utilized strains of rats with low- and high- running capacity (LCR and HCR) and examined learning and memory, DNA synthesis, expression, and post-translational modification of Ogg1 hippocampal cells. Our results showed that rats with higher aerobic/running capacity had better spatial memory, and expressed less Ogg1, when compared to LCR rats. Furthermore, exercise increased SIRT1 expression and decreased acetylated Ogg1 (AcOgg1) levels, a post-translational modification important for efficient repair of 8-oxoG. Our data on cell cultures revealed that nicotinamide, a SIRT1-specific inhibitor, caused the greatest increase in the acetylation of Ogg1, a finding further supported by our other observations that silencing SIRT1 also markedly increased the levels of AcOgg1. These findings imply that high-running capacity is associated with increased hippocampal function, and SIRT1 level/activity and inversely correlates with AcOgg1 levels and thereby the repair of genomic 8-oxoG.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Koltai, Erika
AU - Hart, Nikolett
AU - Taylor, AW
AU - Goto, S
AU - Ngo, JK
AU - Davies, KJ
AU - Radák, Zsolt
TI - Age-associated Declines in Mitochondrial Biogenesis and Protein Quality Control Factors are Minimized by Exercise Training
JF - AMERICAN JOURNAL OF PHYSIOLOGY: REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
J2 - AM J PHYSIOL REG I
VL - 303
PY - 2012
IS - 2
SP - R127
EP - R134
SN - 0363-6119
DO - 10.1152/ajpregu.00337.2011
UR - https://m2.mtmt.hu/api/publication/2006336
ID - 2006336
AB - A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial VO2max, reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (SDH, citrate synthase, COX4, mtDNA), SIRT1 activity, AMPK, pAMPK and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha), UCP3 and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters including NRF1, TFAM, Fis1, Mfn1 and polynucleotide phosphorylase (PNPase) levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Marosi, Krisztina
AU - Felszeghy, Klára
AU - Mehra, R D
AU - Radák, Zsolt
AU - Nyakas, Csaba
TI - Are the neuroprotective effects of estradiol and physical exercise comparable during ageing in female rats?
JF - BIOGERONTOLOGY
J2 - BIOGERONTOLOGY
VL - 13
PY - 2012
IS - 4
SP - 413
EP - 427
PG - 15
SN - 1389-5729
DO - 10.1007/s10522-012-9386-3
UR - https://m2.mtmt.hu/api/publication/2005383
ID - 2005383
AB - Ageing of the brain is accompanied by variable degrees of
cognitive decline. Estrogens have profound effects on brain
ageing by exerting neurotrophic and neuroprotective types of
action. Furthermore, exercise has also been claimed to play a
role in the non-pharmacological prevention of psycho-neuronal
decline with ageing. In the present study the question was asked
whether chronic physical exercise might substitute the action of
estrogens in aged rats. We compared the effects of 17beta-
estradiol (E2) treatment and long-term moderate physical
exercise in ageing (15 months, early stage of ageing) and old
(27 months) female rats, on cognitive functions and the
relevant intracellular molecular signaling pathways in the
hippocampus. Results showed that both treatments improved
attention and memory functions of the 15 months old rats. Like
E2, physical training enhanced the level of brain derived nerve
growth factor and the activation of PKA/Akt/CREB and MAPK/CREB
pathways. The treatments also enhanced the levels of synaptic
molecules synaptophysin and synapsin I, which could explain the
improved cognitive functions. In the 27 months old rats the
behavioral and molecular effects of E2 were indistinguishable
from those found in the 15 months old animals but the effects of
physical exercise in most of the measures proved to be
practically ineffective. It is concluded that the effectiveness
of regular and moderate intensity physical exercise is age-
dependent while the action of E2 treatment is comparable between
the ageing and old female rats on maintaining cognition and its
underlying molecular mechanisms.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Koltai, Erika
AU - Zhao, Z
AU - Lacza, Zsombor
AU - Cselenyák, Attila
AU - Vácz, Gabriella
AU - Nyakas, Csaba
AU - Boldogh, I
AU - Ichinoseki-Sekine, N
AU - Radák, Zsolt
TI - Combined exercise and insulin-like growth factor-1 supplementation induces neurogenesis in old rats, but do not attenuate age-associated DNA damage.
JF - REJUVENATION RESEARCH
J2 - REJUV RES
VL - 14
PY - 2011
IS - 6
SP - 585
EP - 596
PG - 12
SN - 1549-1684
DO - 10.1089/rej.2011.1178
UR - https://m2.mtmt.hu/api/publication/1802845
ID - 1802845
AB - Abstract We have investigated the effects of 2 weeks of insulin-like growth factor-1 (IGF-1) supplementation (5 mug/kg per day) and 6 weeks of exercise training (60% of the maximal oxygen consumption [VO(2) max]) on neurogenesis, DNA damage/repair, and sirtuin content in the hippocampus of young (3 months old) and old (26 months old) rats. Exercise improved the spatial memory of the old group, but IGF-1 supplementation eliminated this effect. An age-associated decrease in neurogenesis was attenuated by exercise and IGF-1 treatment. Aging increased the levels of 8-oxo-7,8-dihydroguanine (8-oxoG) and the protein Ku70, indicating the role of DNA damage in age-related neuropathology. Acetylation of 8-oxoguanine DNA glycosylase (OGG1) was detected in vivo, and this decreased with aging. However, in young animals, exercise and IGF-1 treatment increased acetylated (ac) OGG1 levels. Sirtuin 1 (SIRT1) and SIRT3, as DNA damage-associated lysine deacetylases, were measured, and SIRT1 decreased with aging, resulting in a large increase in acetylated lysine residues in the hippocampus. On the other hand, SIRT3 increased with aging. Exercise-induced neurogenesis might not be a causative factor of increased spatial memory, because IGF-1 plus exercise can induce neurogenesis in the hippocampus of older rats. Data revealed that the age-associated increase in 8-oxoG levels is due to decreased acetylation of OGG1. Age-associated decreases in SIRT1 and the associated increase in lysine acetylation, in the hippocampus, could have significant impact on function and thus, could suggest a therapeutic target.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Koltai, Erika
AU - Szabo, Z
AU - Atalay, M
AU - Boldogh, I
AU - Naito, H
AU - Goto, S
AU - Nyakas, Csaba
AU - Radák, Zsolt
TI - Exercise alters SIRT1, SIRT6, NAD and NAMPT levels in skeletal muscle of aged rats
JF - MECHANISMS OF AGEING AND DEVELOPMENT
J2 - MECH AGEING DEV
VL - 131
PY - 2010
IS - 1
SP - 21
EP - 28
PG - 8
SN - 0047-6374
DO - 10.1016/j.mad.2009.11.002
UR - https://m2.mtmt.hu/api/publication/1303984
ID - 1303984
N1 - Megjegyzés-20894437
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-74149085437&partnerID=40&md5=1ce1443584d504618cb3c1ab8bd664f8
Megjegyzés-20895184
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
74149085437&partnerID=40&md5=1ce1443584d504618cb3c1ab8bd664f8
Megjegyzés-20893971
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-74149085437&partnerID=40&md5=1ce1443584d504618cb3c1ab8bd664f8
AB - Silent information regulators are potent NAD+-dependent protein deacetylases, which have been shown to regulate gene silencing, muscle differentiation and DNA damage repair. Here, changes in the level and activity of sirtuin 1 (SIRT1) in response to exercise in groups of young and old rats were studied. There was an age-related increase in SIRT1 level, while exercise training significantly increased the relative activity of SIRT1. A strong inverse correlation was found between the nuclear activity of SIRT1 and the level of acetylated proteins. Exercise training induced SIRT1 activity due to the positive effect of exercise on the activity of nicotinamide phosphoribosyltransferase (NAMPT) and thereby the production of sirtuin-fueling NAD+. Exercise training normalized the age-associated shift in redox balance, since exercised animals had significantly lower levels of carbonylated proteins, expression of hypoxia-inducible factor-1alpha and vascular endothelial growth factor. The age-associated increase in the level of SIRT6 was attenuated by exercise training. On the other hand, aging did not significantly increase the level of DNA damage, which was in line with the activity of 8-oxoguanine DNA glycosylase, while exercise training increased the level of this enzyme. Regular exercise decelerates the deleterious effects of the aging process via SIRT1-dependent pathways through the stimulation of NAD+ biosynthesis by NAMPT. © 2009 Elsevier Ireland Ltd. All rights reserved.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Marton, Orsolya
AU - Koltai, Erika
AU - Nyakas, Csaba
AU - Bakonyi, Tibor
AU - Zenteno-Savin, T
AU - Kumagai, S
AU - Goto, S
AU - Radák, Zsolt
TI - Aging and exercise affect the level of protein acetylation and SIRT1 activity in cerebellum of male rats
JF - BIOGERONTOLOGY
J2 - BIOGERONTOLOGY
VL - 11
PY - 2010
IS - 6
SP - 679
EP - 686
PG - 8
SN - 1389-5729
DO - 10.1007/s10522-010-9279-2
UR - https://m2.mtmt.hu/api/publication/1405827
ID - 1405827
N1 - Megjegyzés-21114607
Chemicals/CAS: alpha tubulin, 78769-62-7; nicotinamide phosphoribosyltransferase, 9030-27-7;
protein, 67254-75-5
Megjegyzés-21116230
Chemicals/CAS: alpha tubulin, 78769-62-7; nicotinamide phosphoribosyltransferase, 9030-27-7;
protein, 67254-75-5
Megjegyzés-21116358
Chemicals/CAS: alpha tubulin, 78769-62-7; nicotinamide phosphoribosyltransferase, 9030-27-7; protein, 67254-75-5
AB - Aging is associated with a gradual decline in cognitive and motor functions, the result of complex biochemical processes including pre- and posttranslational modifications of proteins. Sirtuins are NAD+ dependent protein deacetylases. These enzymes modulate the aging process by lysine deacetylation, which alters the activity and stability of proteins. Exercise can increase mean life-span and improve quality of life. Data from our laboratories revealed that 4 weeks of treadmill running improves performance in the Morris Maze test for young (4 months, old) but not old (30 months, old) male rats, and the exercise could not prevent the age-associated loss in muscle strength assessed by a gripping test. The positive correlation between protein acetylation and the gripping test suggests that the age-dependent decrease in relative activity of SIRT1 in the cerebellum impairs motor function. Similarly to the acetylation level of total proteins, the acetylation of α′-tubulin is also increased with aging, while the effect of exercise training was not found to be significant. Moreover, the protein content of nicotinamide phosphoribosyltransferase, one of the key enzymes of NAD biosynthesis, decreased in the young exercise group. These data suggest that aging results in decreased specific activity of SIRT1 in cerebellum, which could lead to increased acetylation of protein residues, including α′-tubulin, that interfere with motor function. © 2010 Springer Science+Business Media B.V.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Radák, Zsolt
AU - Boldogh, I
TI - 8-Oxo-7,8-dihydroguanine: Links to gene expression, aging, and defense against oxidative stress
JF - FREE RADICAL BIOLOGY AND MEDICINE
J2 - FREE RADICAL BIO MED
VL - 49
PY - 2010
IS - 4
SP - 587
EP - 596
PG - 10
SN - 0891-5849
DO - 10.1016/j.freeradbiomed.2010.05.008
UR - https://m2.mtmt.hu/api/publication/1405829
ID - 1405829
N1 - Megjegyzés-21114612
Chemicals/CAS: 8 hydroxyguanine, 5614-64-2; DNA glycosyltransferase, 70356-40-0; guanine, 69257-39-2, 73-40-5
Megjegyzés-21114652
Chemicals/CAS: 8 hydroxyguanine, 5614-64-2; DNA glycosyltransferase, 70356-40-0; guanine, 69257-
39-2, 73-40-5
Megjegyzés-21115357
Chemicals/CAS: 8 hydroxyguanine, 5614-64-2; DNA glycosyltransferase, 70356-40-0; guanine, 69257-39-2, 73-40-5
Megjegyzés-21116046
Chemicals/CAS: 8 hydroxyguanine, 5614-64-2; DNA glycosyltransferase, 70356-40-0; guanine, 69257-39-2, 73-40-5
Megjegyzés-21112678
Chemicals/CAS: 8 hydroxyguanine, 5614-64-2; DNA glycosyltransferase, 70356-40-0; guanine, 69257-
39-2, 73-40-5
AB - The one-electron oxidation product of guanine, 8-oxo-7,8-dihydroguanine (8-oxoG), is an abundant lesion in genomic, mitochondrial, and telomeric DNA and RNA. It is considered to be a marker of oxidative stress that preferentially accumulates at the 5' end of guanine strings in the DNA helix, in guanine quadruplexes, and in RNA molecules. 8-OxoG has a lower oxidation potential compared to guanine; thus it is susceptible to oxidation/reduction and, along with its redox products, is traditionally considered to be a major mutagenic DNA base lesion. It does not change the architecture of the DNA double helix and it is specifically recognized and excised by 8-oxoguanine DNA glycosylase (OGG1) during the DNA base excision repair pathway. OGG1 null animals accumulate excess levels of 8-oxoG in their genome, yet they do not have shorter life span nor do they exhibit severe pathological symptoms including tumor formation. In fact they are increasingly resistant to inflammation. Here we address the rarely considered significance of 8-oxoG, such as its optimal levels in DNA and RNA under a given condition, essentiality for normal cellular physiology, evolutionary role, and ability to soften the effects of oxidative stress in DNA, and the harmful consequences of its repair, as well as its importance in transcriptional initiation and chromatin relaxation. © 2010 Elsevier Inc.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Csiszar, Anna
AU - Labinskyy, N
AU - Pinto, JT
AU - Ballabh, P
AU - Zhang, HR
AU - Losonczy, György
AU - Pearson, K
AU - de Cabo, R
AU - Pacher, Pál
AU - Zhang, CH
AU - Ungvári, Zoltán István
TI - Resveratrol induces mitochondrial biogenesis in endothelial cells
JF - AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY
J2 - AM J PHYSIOL HEART C
VL - 297
PY - 2009
IS - 1
SP - H13
EP - H20
SN - 0363-6135
DO - 10.1152/ajpheart.00368.2009
UR - https://m2.mtmt.hu/api/publication/1416570
ID - 1416570
AB - Csiszar A, Labinskyy N, Pinto JT, Ballabh P, Zhang H, Losonczy G, Pearson K, de Cabo R, Pacher P, Zhang C, Ungvari Z. Resveratrol induces mitochondrial biogenesis in endothelial cells. Am J Physiol Heart Circ Physiol 297: H13-H20, 2009. First published May 8, 2009; doi:10.1152/ajpheart.00368.2009.-Pathways that regulate mitochondrial biogenesis are potential therapeutic targets for the amelioration of endothelial dysfunction and vascular disease. Resveratrol was shown to impact mitochondrial function in skeletal muscle and the liver, but its role in mitochondrial biogenesis in endothelial cells remains poorly defined. The present study determined whether resveratrol induces mitochondrial biogenesis in cultured human coronary arterial endothelial cells (CAECs). In CAECs resveratrol increased mitochondrial mass and mitochondrial DNA content, upregulated protein expression of electron transport chain constituents, and induced mitochondrial biogenesis factors (proliferator-activated receptor-coactivator-1 alpha, nuclear respiratory factor-1, mitochondrial transcription factor A). Sirtuin 1 (SIRT1) was induced, and endothelial nitric oxide (NO) synthase (eNOS) was upregulated in a SIRT1-dependent manner. Knockdown of SIRT1 (small interfering RNA) or inhibition of NO synthesis prevented resveratrol-induced mitochondrial biogenesis. In aortas of type 2 diabetic (db/db) mice impaired mitochondrial biogenesis was normalized by chronic resveratrol treatment, showing the in vivo relevance of our findings. Resveratrol increases mitochondrial content in endothelial cells via activating SIRT1. We propose that SIRT1, via a pathway that involves the upregulation of eNOS, induces mitochondrial biogenesis. Resveratrol induced mitochondrial biogenesis in the aortas of type 2 diabetic mice, suggesting the potential for new treatment approaches targeting endothelial mitochondria in metabolic diseases.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Siamilis, S
AU - Jakus, Judit
AU - Nyakas, Csaba
AU - Costa, A
AU - Mihalik, B
AU - Falus, András
AU - Radák, Zsolt
TI - The effect of exercise and oxidant-antioxidant intervention on the levels of neurotrophins and free radicals in spinal cord of rats
JF - SPINAL CORD
J2 - SPINAL CORD
VL - 47
PY - 2009
IS - 6
SP - 453
EP - 457
PG - 5
SN - 1362-4393
DO - 10.1038/sc.2008.125
UR - https://m2.mtmt.hu/api/publication/1303988
ID - 1303988
N1 - Megjegyzés-20894641
PubMed ID: 18936770
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; hydrogen peroxide, 7722-84-1; n tert butyl alpha phenylnitrone, 3376-24-7; sodium chloride, 7647-14-5; Antioxidants; Brain-Derived Neurotrophic Factor; Cyclic N-Oxides; Free Radicals; Glial Cell Line-Derived Neurotrophic Factor; Hydrogen Peroxide, 7722-84-1; Nerve Growth Factors; Oxidants; RNA, Messenger; phenyl-N-tert-butylnitrone, 3376-24-7
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-67651124879&partnerID=40&md5=db42f99c1f9fa9dcd43d04637da206a8
Megjegyzés-20895047
PubMed ID: 18936770
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; hydrogen peroxide, 7722-84-1; n
tert butyl alpha phenylnitrone, 3376-24-7; sodium chloride, 7647-14-5; Antioxidants; Brain-
Derived Neurotrophic Factor; Cyclic N-Oxides; Free Radicals; Glial Cell Line-Derived
Neurotrophic Factor; Hydrogen Peroxide, 7722-84-1; Nerve Growth Factors; Oxidants; RNA,
Messenger; phenyl-N-tert-butylnitrone, 3376-24-7
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
67651124879&partnerID=40&md5=db42f99c1f9fa9dcd43d04637da206a8
Megjegyzés-21115275
PubMed ID: 18936770
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; hydrogen peroxide, 7722-84-1; n
tert butyl alpha phenylnitrone, 3376-24-7; sodium chloride, 7647-14-5; Antioxidants; Brain-
Derived Neurotrophic Factor; Cyclic N-Oxides; Free Radicals; Glial Cell Line-Derived
Neurotrophic Factor; Hydrogen Peroxide, 7722-84-1; Nerve Growth Factors; Oxidants; RNA,
Messenger; phenyl-N-tert-butylnitrone, 3376-24-7
Megjegyzés-20893287
PubMed ID: 18936770
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; hydrogen peroxide, 7722-84-1; n
tert butyl alpha phenylnitrone, 3376-24-7; sodium chloride, 7647-14-5; Antioxidants; Brain-
Derived Neurotrophic Factor; Cyclic N-Oxides; Free Radicals; Glial Cell Line-Derived
Neurotrophic Factor; Hydrogen Peroxide, 7722-84-1; Nerve Growth Factors; Oxidants; RNA,
Messenger; phenyl-N-tert-butylnitrone, 3376-24-7
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
67651124879&partnerID=40&md5=db42f99c1f9fa9dcd43d04637da206a8
AB - Study design: This study was designed to investigate the effects
of oxidant and antioxidant treatment, as well as regular
exercise, on neurotrophin levels in the spinal cord of rats.
Objectives: Reactive oxygen species (ROS) play a role in
neurodegenerative diseases, but ROS at moderate levels could
stimulate biochemical processes through redox-sensitive
transcription. Methods: Exercised or sedentary animals were
injected subcutaneously with hydrogen peroxide (H 2 O 2), N-tert
butyl-α-phenyl nitrone (PBN) or saline for the last 2 weeks of a
10-week experimental period to challenge redox balance. Free
radical (FR) concentration was evaluated in the spinal cord by
electron spin resonance, protein carbonyls, brain-derived
neurotrophic factor (BDNF), glial cell line-derived neurotrophic
factor (GDNF) levels and the mRNA expression of BDNF receptor
and tyrosine kinase receptor B (TrKB). Setting: Research
Institute of Sport Science, Semmelweis University, Budapest,
Hungary. Results: Exercise or PBN decreased the concentration of
FR, whereas the carbonyl content did not change. BDNF was
significantly decreased in exercised sham and sedentary PBN-
treated groups, and its content correlated with the level of FR.
GDNF was significantly increased in sedentary H 2 O 2 -treated
groups. No differences were observed in TrkB mRNA expression
among groups. Conclusions: Results suggest that regular exercise
alone and PBN in sedentary animals can successfully decrease FR
levels in the spinal cord. Redox alteration seems to affect the
levels of GDNF and BDNF, which might have clinical consequences,
as neurotrophins play an important role in cellular resistance
and regeneration. © 2009 International Spinal Cord Society All
rights reserved.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Radák, Zsolt
AU - Chung, H Y
AU - Goto, S
TI - Systemic adaptation to oxidative challenge induced by regular exercise
JF - FREE RADICAL BIOLOGY AND MEDICINE
J2 - FREE RADICAL BIO MED
VL - 44
PY - 2008
IS - 2
SP - 153
EP - 159
PG - 7
SN - 0891-5849
DO - 10.1016/j.freeradbiomed.2007.01.029
UR - https://m2.mtmt.hu/api/publication/1303995
ID - 1303995
N1 - Megjegyzés-20892799
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
Megjegyzés-20892815
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20892856
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20893128
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-
5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
Megjegyzés-20893235
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-
5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20893262
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-
5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20893307
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-
5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20893341
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-
5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20893931
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20893980
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20894111
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20894448
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20894529
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20894651
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20894727
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-20894757
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-37849004479&partnerID=40&md5=2d0114e1bd5632cb900a6f3c30dc2571
Megjegyzés-21115287
PubMed ID: 18191751
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; glutathione peroxidase, 9013-66-5;
superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; xanthine dehydrogenase, 9054-84-6
Admin megjegyzés-22433966
Scopusban nem szerepel az idézett művek között. DOI fulltextből lett megállapítva az idézés ténye.
WOS-ban pedig 'in press'-ként szerepel az idézett művek között.
A DOI-n is 'in press'-ként van feltüntetve az idézett mű.
AB - Exercise is associated with increased ATP need and an enhanced aerobic and/or anaerobic metabolism, which results in an increased formation of reactive oxygen species (ROS). Regular exercise seems to decrease the incidence of a wide range of ROS-associated diseases, including heart disease, type II diabetes, rheumatic arthritis, Alzheimer and Parkinson diseases, and certain cancers. The preventive effect of regular exercise, at least in part, is due to oxidative stress-induced adaptation. The oxidative challenge-related adaptive process of exercise is probably not just dependent upon the generated level of ROS but primarily on the increase in antioxidant and housekeeping enzyme activities, which involves the oxidative damage repair enzymes. Therefore, the effects of exercise resemble the characteristics of hormesis. In addition, it seems that the oxidative challenge-related effects of exercise are systemic. Skeletal muscle, liver, and brain have very different metabolic rates and functions during exercise, but the adaptive response is very similar: increased antioxidant/damage repair enzyme activity, lower oxidative damage, and increased resistance to oxidative stress, due to the changes in redox homeostasis. Hence, it is highly possible that the well-known beneficial effects of exercise are due to the capability of exercise to produce increased levels of ROS. Or in other words, it seems that the vulnerability of the body to oxidative stress and diseases is significantly enhanced in a sedentary compared to a physically active lifestyle. © 2007 Elsevier Inc. All rights reserved.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Radák, Zsolt
AU - Toldy, A
AU - Szabó, Zs
AU - Siamilis, S
AU - Nyakas, Csaba
AU - Silye, G
AU - Jakus, Judit
AU - Goto, S
TI - The effects of training and detraining on memory, neurotrophins and oxidative stress markers in rat brain
JF - NEUROCHEMISTRY INTERNATIONAL
J2 - NEUROCHEM INT
VL - 49
PY - 2006
IS - 4
SP - 387
EP - 392
PG - 6
SN - 0197-0186
DO - 10.1016/j.neuint.2006.02.004
UR - https://m2.mtmt.hu/api/publication/112944
ID - 112944
N1 - Megjegyzés-20592721
PubMed ID: 16564605
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; nerve growth factor, 9061-61-4; Biological Markers; Brain-Derived Neurotrophic Factor; DNA Glycosylases, EC 3.2.2.-; Nerve Growth Factors; Nuclear Proteins; OGG1 protein, rat, EC 3.2.2.-; Proteasome Endopeptidase Complex, EC 3.4.25.1
Megjegyzés-20893266
PubMed ID: 16564605
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; nerve growth factor, 9061-61-4;
Biological Markers; Brain-Derived Neurotrophic Factor; DNA Glycosylases, EC 3.2.2.-; Nerve
Growth Factors; Nuclear Proteins; OGG1 protein, rat, EC 3.2.2.-; Proteasome Endopeptidase
Complex, EC 3.4.25.1
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
33746378378&partnerID=40&md5=a8af0bd5c1f419403d1b60e646b1f54a
Megjegyzés-20893962
PubMed ID: 16564605
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; nerve growth factor, 9061-61-4; Biological Markers; Brain-Derived Neurotrophic Factor; DNA Glycosylases, EC 3.2.2.-; Nerve Growth Factors; Nuclear Proteins; OGG1 protein, rat, EC 3.2.2.-; Proteasome Endopeptidase Complex, EC 3.4.25.1
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-33746378378&partnerID=40&md5=a8af0bd5c1f419403d1b60e646b1f54a
Megjegyzés-20894001
PubMed ID: 16564605
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; nerve growth factor, 9061-61-4; Biological Markers; Brain-Derived Neurotrophic Factor; DNA Glycosylases, EC 3.2.2.-; Nerve Growth Factors; Nuclear Proteins; OGG1 protein, rat, EC 3.2.2.-; Proteasome Endopeptidase Complex, EC 3.4.25.1
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-33746378378&partnerID=40&md5=a8af0bd5c1f419403d1b60e646b1f54a
Megjegyzés-20894468
PubMed ID: 16564605
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; nerve growth factor, 9061-61-4; Biological Markers; Brain-Derived Neurotrophic Factor; DNA Glycosylases, EC 3.2.2.-; Nerve Growth Factors; Nuclear Proteins; OGG1 protein, rat, EC 3.2.2.-; Proteasome Endopeptidase Complex, EC 3.4.25.1
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-33746378378&partnerID=40&md5=a8af0bd5c1f419403d1b60e646b1f54a
Megjegyzés-20894680
PubMed ID: 16564605
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; nerve growth factor, 9061-61-4; Biological Markers; Brain-Derived Neurotrophic Factor; DNA Glycosylases, EC 3.2.2.-; Nerve Growth Factors; Nuclear Proteins; OGG1 protein, rat, EC 3.2.2.-; Proteasome Endopeptidase Complex, EC 3.4.25.1
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-33746378378&partnerID=40&md5=a8af0bd5c1f419403d1b60e646b1f54a
Megjegyzés-20894773
PubMed ID: 16564605
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; nerve growth factor, 9061-61-4; Biological Markers; Brain-Derived Neurotrophic Factor; DNA Glycosylases, EC 3.2.2.-; Nerve Growth Factors; Nuclear Proteins; OGG1 protein, rat, EC 3.2.2.-; Proteasome Endopeptidase Complex, EC 3.4.25.1
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-33746378378&partnerID=40&md5=a8af0bd5c1f419403d1b60e646b1f54a
Megjegyzés-21116235
PubMed ID: 16564605
Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; nerve growth factor, 9061-61-4;
Biological Markers; Brain-Derived Neurotrophic Factor; DNA Glycosylases, EC 3.2.2.-; Nerve
Growth Factors; Nuclear Proteins; OGG1 protein, rat, EC 3.2.2.-; Proteasome Endopeptidase
Complex, EC 3.4.25.1
AB - In the current investigation we tested how swimming training (T) (8 week, 5 times/week, 2 h/day), and detraining (DT) affects brain functions and oxidative stress markers in rat brain. The free radical concentration, measured by electron paramagnetic resonance, decreased in brain of T and DT rats compared to controls (C). The level of brain-derived neurotrophic factor (BDNF) increased as a result of training, but decreased below the control level after 6 weeks of detraining. In addition, the concentration of nerve growth factor (NGF) also declined with DT. The passive avoidance test was used to assess the memory of rats, and training-induced improvement was observed but the enhancement disappeared with detraining. When the content of mitochondrial electron transport complexes, as a potent free radical generator, was evaluated by the blue native gel method, no significant alterations were observed. The repair of nuclear and mitochondrial 8-oxodeoxyguanosine, as measured by the activity of OGGI, showed no significant difference. Therefore, the results suggest that regular exercise training improves memory, decreases the level of reactive oxygen species, and increase the production of BDNF and NGR On the other hand, it appears that the beneficial effects of training are reversible in the brain, since detraining down-regulates the neurotrophin level, and memory. It is suggested that exercise training is more likely to beneficially effect the production of reactive oxygen species and the related oxidative damage. (c) 2006 Elsevier Ltd. All rights reserved.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Radák, Zsolt
AU - Taylor, A W
AU - Ohno, H
AU - Goto, S
TI - Adaptation to exercise-induced oxidative stress: From muscle to brain
JF - EXERCISE IMMUNOLOGY REVIEW
J2 - EXERC IMMUNOL REV
VL - 7
PY - 2001
SP - 90
EP - 107
PG - 18
SN - 1077-5552
UR - https://m2.mtmt.hu/api/publication/1304018
ID - 1304018
N1 - Megjegyzés-20892838
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
Megjegyzés-20893257
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
Megjegyzés-20893282
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
0034813092&partnerID=40&md5=26837ee3807b14d3d5ab93837cd45682
Megjegyzés-20893367
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-
0034813092&partnerID=40&md5=26837ee3807b14d3d5ab93837cd45682
Megjegyzés-21116284
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
Megjegyzés-21116596
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
Megjegyzés-20892805
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
Megjegyzés-20893215
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-0034813092&partnerID=40&md5=26837ee3807b14d3d5ab93837cd45682
Megjegyzés-20893414
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-0034813092&partnerID=40&md5=26837ee3807b14d3d5ab93837cd45682
Megjegyzés-20894561
PubMed ID: 11579750
Chemicals/CAS: Reactive Nitrogen Species; Reactive Oxygen Species
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-0034813092&partnerID=40&md5=26837ee3807b14d3d5ab93837cd45682
AB - Exercise increases the generation of reactive oxygen and nitrogen species (RONS) and by causing adaptation, could decrease the incidence of RONS-associated diseases. A single bout of exercise, depending upon intensity and duration, can cause an increase in antioxidant enzyme activity, decrease levels of thiols and antioxidant vitamins, and result in oxidative damage as a sign of incomplete adaptation. Increased levels of RONS and oxidative damage are initiators of a specific adaptive response, such as the stimulation of the activation of antioxidant enzymes, thiols, and enhanced oxidative damage repair. Regular exercise has the capability to develop compensation to oxidative stress, resulting in overcompensation against the increased level of RONS production and oxidative damage. Regular exercise causes adaptation of the antioxidant and repair systems, which could result in a decreased base level of oxidative damage and increased resistance to oxidative stress.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Radák, Zsolt
AU - Kaneko, T
AU - Tahara, S
AU - Nakamoto, H
AU - Pucsok, J
AU - Sasvári, M
AU - Nyakas, Csaba
AU - Goto, S
TI - Regular exercise improves cognitive function and decreases oxidative damage in rat brain
JF - NEUROCHEMISTRY INTERNATIONAL
J2 - NEUROCHEM INT
VL - 38
PY - 2001
IS - 1
SP - 17
EP - 23
PG - 7
SN - 0197-0186
DO - 10.1016/S0197-0186(00)00063-2
UR - https://m2.mtmt.hu/api/publication/1304021
ID - 1304021
N1 - Megjegyzés-20892804
PubMed ID: 10913684
Chemicals/CAS: Citrate (si)-Synthase, EC 2.3.3.1; Cysteine Endopeptidases, EC 3.4.22.-; Multienzyme Complexes; Nerve Tissue Proteins; Proteasome Endopeptidase Complex, EC 3.4.25.1; Thiobarbituric Acid Reactive Substances
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-0035241612&partnerID=40&md5=6027753d85772f01a3014ff0289ebe0c
Megjegyzés-20892884
PubMed ID: 10913684
Chemicals/CAS: Citrate (si)-Synthase, EC 2.3.3.1; Cysteine Endopeptidases, EC 3.4.22.-; Multienzyme Complexes; Nerve Tissue Proteins; Proteasome Endopeptidase Complex, EC 3.4.25.1; Thiobarbituric Acid Reactive Substances
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-0035241612&partnerID=40&md5=6027753d85772f01a3014ff0289ebe0c
Megjegyzés-20892951
PubMed ID: 10913684
Chemicals/CAS: Citrate (si)-Synthase, EC 2.3.3.1; Cysteine Endopeptidases, EC 3.4.22.-; Multienzyme Complexes; Nerve Tissue Proteins; Proteasome Endopeptidase Complex, EC 3.4.25.1; Thiobarbituric Acid Reactive Substances
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-0035241612&partnerID=40&md5=6027753d85772f01a3014ff0289ebe0c
Megjegyzés-20894557
PubMed ID: 10913684
Chemicals/CAS: Citrate (si)-Synthase, EC 2.3.3.1; Cysteine Endopeptidases, EC 3.4.22.-; Multienzyme Complexes; Nerve Tissue Proteins; Proteasome Endopeptidase Complex, EC 3.4.25.1; Thiobarbituric Acid Reactive Substances
UR: http://www.scopus.com/inward/record.url?eid=2-s2.0-0035241612&partnerID=40&md5=6027753d85772f01a3014ff0289ebe0c
Megjegyzés-21116590
PubMed ID: 10913684
Chemicals/CAS: Citrate (si)-Synthase, EC 2.3.3.1; Cysteine Endopeptidases, EC 3.4.22.-;
Multienzyme Complexes; Nerve Tissue Proteins; Proteasome Endopeptidase Complex, EC 3.4.25.1;
Thiobarbituric Acid Reactive Substances
AB - The biochemical mechanisms by which regular exercise significantly benefits health and well being, including improved cognitive function, are not well understood. Four-week-old (young) and 14-month-old (middle aged) Wistar rats were randomly assigned to young control and young exercised, middle-aged control and middle-aged exercised groups. Exercise groups were exposed to a swimming regime of 1 h a day, 5 days a week for 9 weeks. The passive avoidance test showed that middle-aged exercised rats had significantly (P<0.05) better short- (24 h) and long-term (72 h) memory than aged-matched control rats. Conditioned pole-jumping avoidance learning was improved markedly in both age groups by exercise. Brain thiobarbituric acid-reactive substances and 8-hydroxy-2'deoxyguanosine content in the DNA did not change significantly, while the protein carbonyl levels decreased significantly (P<0.05) in both exercised groups. This decrease was accompanied by an increase in the chymotrypsin-like activity of proteasome complex in the exercised groups, whereas trypsin-like activity did not differ significantly between all groups. The DT-diaphorase activity increased significantly (P<0.05) in the brain of young exercised animals. These data show that swimming training improves some cognitive functions in rats, with parallel attenuation of the accumulation of oxidatively damaged proteins. Copyright (C) 2000 Elsevier Science Ltd.
LA - English
DB - MTMT
ER -