@article{MTMT:32613311,
	title = {Astaxanthin Exerts Anabolic Effects via Pleiotropic Modulation of the Excitable Tissue},
	url = {https://m2.mtmt.hu/api/publication/32613311},
	author = {Gönczi, Mónika and Csemer, Andrea and Szabó, László and Sztretye, Mónika and Fodor, János and Deák-Pocsai, Krisztina and Szenthe, Kálmán and Keller-Pintér, Anikó and Köhler, Zoltán Márton and Nánási, Péter Pál and Szentandrássy, Norbert and Pál, Balázs Zoltán and Csernoch, László},
	doi = {10.3390/ijms23020917},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32613311},
	issn = {1661-6596},
	abstract = {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.},
	keywords = {skeletal muscle; Gene Expression; food intake; Excitability; Cardiac action potential; INHIBITORY POSTSYNAPTIC CURRENT; astaxanthin (ASTA); arcuate nucleus},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Keller-Pintér, Anikó/0000-0002-4105-8458; Köhler, Zoltán Márton/0000-0002-8299-105X; Szentandrássy, Norbert/0000-0003-0197-9567}
}

@article{MTMT:31145381,
	title = {Improved Tetanic Force and Mitochondrial Calcium Homeostasis by Astaxanthin Treatment in Mouse Skeletal Muscle},
	url = {https://m2.mtmt.hu/api/publication/31145381},
	author = {Sztretye, Mónika and Singlár, Zoltán and Szabó, László and Angyal, Ágnes and Balogh, Norbert and Vakilzadeh, Faranak and Szentesi, Péter and Dienes, Beatrix and Csernoch, László},
	doi = {10.3390/antiox9020098},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {9},
	unique-id = {31145381},
	abstract = {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.},
	year = {2020},
	eissn = {2076-3921},
	orcid-numbers = {Szentesi, Péter/0000-0003-2621-2282}
}

@article{MTMT:30814023,
	title = {Astaxanthin: A Potential Mitochondrial-Targeted Antioxidant Treatment in Diseases and with Aging},
	url = {https://m2.mtmt.hu/api/publication/30814023},
	author = {Sztretye, Mónika and Dienes, Beatrix and Gönczi, Mónika and Czirják, Tamás and Csernoch, László and Dux, László and Szentesi, Péter and Keller-Pintér, Anikó},
	doi = {10.1155/2019/3849692},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2019},
	unique-id = {30814023},
	issn = {1942-0900},
	abstract = {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.},
	year = {2019},
	eissn = {1942-0994},
	orcid-numbers = {Dux, László/0000-0002-1270-1678; Szentesi, Péter/0000-0003-2621-2282; Keller-Pintér, Anikó/0000-0002-4105-8458}
}