TY - JOUR AU - Gönczi, Mónika AU - Csemer, Andrea AU - Szabó, László AU - Sztretye, Mónika AU - Fodor, János AU - Deák-Pocsai, Krisztina AU - Szenthe, Kálmán AU - Keller-Pintér, Anikó AU - Köhler, Zoltán Márton AU - Nánási, Péter Pál AU - Szentandrássy, Norbert AU - Pál, Balázs Zoltán AU - Csernoch, László TI - Astaxanthin Exerts Anabolic Effects via Pleiotropic Modulation of the Excitable Tissue JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 2 PG - 19 SN - 1661-6596 DO - 10.3390/ijms23020917 UR - https://m2.mtmt.hu/api/publication/32613311 ID - 32613311 N1 - Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, 4012, Hungary Doctoral School of Molecular Medicine, University of Debrecen, Debrecen, 4012, Hungary Carlsbad Research Organization Ltd, Újrónafő, 9244, Hungary Department of Biochemistry, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Dental Physiology and Pharmacology, Faculty of Dentistry, University of Debrecen, Debrecen, 4012, Hungary Department of Basic Medical Sciences, Faculty of Dentistry, University of Debrecen, Debrecen, 4012, Hungary Export Date: 2 March 2023 Correspondence Address: Pál, B.; Department of Physiology, Hungary; email: pal.balazs@med.unideb.hu Chemicals/CAS: acyl coenzyme A desaturase, 9014-34-0; astaxanthin, 472-61-7; carbon dioxide, 124-38-9, 58561-67-4; fatty acid synthase, 9045-77-6; ketamine, 1867-66-9, 6740-88-1, 81771-21-3; xanthine dehydrogenase, 9054-84-6; xylazine, 23076-35-9, 7361-61-7; xanthophyll, 127-40-2, 52842-48-5; Anabolic Agents; astaxanthine; Xanthophylls Tradenames: calypsol, Richter, Hungary; sedaxylan, Eurovet, Netherlands Manufacturers: Richter, Hungary; Eurovet, Netherlands Funding details: AstaReal A1010 Funding details: TKP-2020-NKA-04 Funding details: 2020-4.1.1-TKP2020 Funding details: Magyar Tudományos Akadémia, MTA, EFOP-3.6.2-16-2017-00006, EFOP-3.6.3-VEKOP-16-2017-00009, TKP2020-IKA-04 Funding details: Debreceni Egyetem, DE Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH, FK 134684, GINOP-2.3.2-15-2016-00040, GINOP-2.3.3.15-2016-00020, NKFIH-K115397, NKFIH-K138090, PD-128370 Funding text 1: Funding: This research was supported by the National Research, Development and Innovation Office of Hungary (grant numbers: GINOP-2.3.2-15-2016-00040 (MYOTeam), GINOP-2.3.3.15-2016-00020, NKFI FK 134684 (A.K.-P), NKFIH PD-128370 (M.S.), NKFIH-K115397 (P.N.), NKFIH-K138090 (N.S.)) and the János Bolyai Research Scholarship of the Hungarian Academy of Sciences (to A.K.-P.). This work was also supported by the project EFOP-3.6.3-VEKOP-16-2017-00009 (M.S.) and EFOP-3.6.2-16-2017-00006 (P.N.). Project no. TKP2020-IKA-04 was implemented with the support provided from the National Research, Development and Innovation Fund of Hungary, financed under the 2020-4.1.1-TKP2020 funding scheme. Support was also obtained from the Thematic Excellence Program of the Ministry for Innovation and Technology in Hungary (TKP-2020-NKA-04), within the framework of the Space Sciences thematic program of the University of Debrecen. Funding text 2: This research was supported by the National Research, Development and Innovation Office of Hungary (grant numbers: GINOP-2.3.2-15-2016-00040 (MYOTeam), GINOP-2.3.3.15-2016-00020, NKFI FK 134684 (A.K.-P), NKFIH PD-128370 (M.S.), NKFIH-K115397 (P.N.), NKFIH-K138090 (N.S.)) and the J?nos Bolyai Research Scholarship of the Hungarian Academy of Sciences (to A.K.-P.). This work was also supported by the project EFOP-3.6.3-VEKOP-16-2017-00009 (M.S.) and EFOP-3.6.2-16-2017-00006 (P.N.). Project no. TKP2020-IKA-04 was implemented with the support provided from the National Research, Development and Innovation Fund of Hungary, financed under the 2020-4.1.1-TKP2020 funding scheme. Support was also obtained from the Thematic Excellence Program of the Ministry for Innovation and Technology in Hungary (TKP-2020-NKA-04), within the framework of the Space Sciences thematic program of the University of Debrecen.Acknowledgments: The authors are indebted to ?va S?gi and Tamara L?vei for their excellent technical assistance. We are grateful to AstaReal Co., Ltd., (Nacka, Sweden) for providing astaxanthin (AstaReal A1010) for research purposes. AB - Astaxanthin is a lipid-soluble carotenoid influencing lipid metabolism, body weight, and insulin sensitivity. We provide a systematic analysis of acute and chronic effects of astaxanthin on different organs. Changes by chronic astaxanthin feeding were analyzed on general metabolism, expression of regulatory proteins in the skeletal muscle, as well as changes of excitation and synaptic activity in the hypothalamic arcuate nucleus of mice. Acute responses were also tested on canine cardiac muscle and different neuronal populations of the hypothalamic arcuate nucleus in mice. Dietary astaxanthin significantly increased food intake. It also increased protein levels affecting glucose metabolism and fatty acid biosynthesis in skeletal muscle. Inhibitory inputs innervating neurons of the arcuate nucleus regulating metabolism and food intake were strengthened by both acute and chronic astaxanthin treatment. Astaxanthin moderately shortened cardiac action potentials, depressed their plateau potential, and reduced the maximal rate of depolarization. Based on its complex actions on metabolism and food intake, our data support the previous findings that astaxanthin is suitable for supplementing the diet of patients with disturbances in energy homeostasis. LA - English DB - MTMT ER - TY - JOUR AU - Sztretye, Mónika AU - Singlár, Zoltán AU - Szabó, László AU - Angyal, Ágnes AU - Balogh, Norbert AU - Vakilzadeh, Faranak AU - Szentesi, Péter AU - Dienes, Beatrix AU - Csernoch, László TI - Improved Tetanic Force and Mitochondrial Calcium Homeostasis by Astaxanthin Treatment in Mouse Skeletal Muscle JF - ANTIOXIDANTS J2 - ANTIOXIDANTS-BASEL VL - 9 PY - 2020 IS - 2 PG - 17 SN - 2076-3921 DO - 10.3390/antiox9020098 UR - https://m2.mtmt.hu/api/publication/31145381 ID - 31145381 AB - Background: Astaxanthin (AX) a marine carotenoid is a powerful natural antioxidant which protects against oxidative stress and improves muscle performance. Retinol and its derivatives were described to affect lipid and energy metabolism. Up to date, the effects of AX and retinol on excitation-contraction coupling (ECC) in skeletal muscle are poorly described. Methods: 18 C57Bl6 mice were divided into two groups: Control and AX supplemented in rodent chow for 4 weeks (AstaReal A1010). In vivo and in vitro force and intracellular calcium homeostasis was studied. In some experiments acute treatment with retinol was employed. Results: The voltage activation of calcium transients (V50) were investigated in single flexor digitorum brevis isolated fibers under patch clamp and no significant changes were found following AX supplementation. Retinol shifted V50 towards more positive values and decreased the peak F/F0 of the calcium transients. The amplitude of tetani in the extensor digitorum longus was significantly higher in AX than in control group. Lastly, the mitochondrial calcium uptake was found to be less prominent in AX. Conclusion: AX supplementation increases in vitro tetanic force without affecting ECC and exerts a protecting effect on the mitochondria. Retinol treatment has an inhibitory effect on ECC in skeletal muscle. LA - English DB - MTMT ER - TY - JOUR AU - Sztretye, Mónika AU - Dienes, Beatrix AU - Gönczi, Mónika AU - Czirják, Tamás AU - Csernoch, László AU - Dux, László AU - Szentesi, Péter AU - Keller-Pintér, Anikó TI - Astaxanthin: A Potential Mitochondrial-Targeted Antioxidant Treatment in Diseases and with Aging JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2019 PY - 2019 PG - 14 SN - 1942-0900 DO - 10.1155/2019/3849692 UR - https://m2.mtmt.hu/api/publication/30814023 ID - 30814023 N1 - A real.mtak-ról letölhető pdf neve (Astaxanthinreview_revised_2019.pdf) alapján az ott található egy revised változat, melynek bibliográfiai leírása eltér az újságban megjelent, hivatalos változat leírásától. A leírásban eltérések: A hivatalos megjelenés (a folyóirat) szerint a pontos cím: "Astaxanthin: A Potential Mitochondrial-Targeted Antioxidant Treatment in Diseases and with Aging", míg az real.mtak leírása szerint a pontos cím: "Astaxanthin, a potential mitochondrial targeted antioxidant treatment in diseases and with aging". A real.mtak szerinti leírás, a revised változat szerint a 200.kötetben a 1-28. oldalon található, a hivatalos megjelenés (a folyóirat) szerint a 2019. évi kötetben a 14 oldalas terjedelemben található. Továbbá az absztraktban is található egy minimális eltérés ( pl.: a revised változatban prooxidant helyett pro-oxidant szerepel, vagy az and helyett as well as szerepel a mondatban, stb.). AB - Oxidative stress is characterized by an imbalance between prooxidant and antioxidant species, leading to macromolecular damage and disruption of redox signaling and cellular control. It is a hallmark of various diseases including metabolic syndrome, chronic fatigue syndrome, neurodegenerative, cardiovascular, inflammatory, and age-related diseases. Several mitochondrial defects have been considered to contribute to the development of oxidative stress and known as the major mediators of the aging process and subsequent age-associated diseases. Thus, mitochondrial-targeted antioxidants should prevent or slow down these processes and prolong longevity. This is the reason why antioxidant treatments are extensively studied and newer and newer compounds with such an effect appear. Astaxanthin, a xanthophyll carotenoid, is the most abundant carotenoid in marine organisms and is one of the most powerful natural compounds with remarkable antioxidant activity. Here, we summarize its antioxidant targets, effects, and benefits in diseases and with aging. LA - English DB - MTMT ER -