L-Methionine Protects against Oxidative Stress and Mitochondrial Dysfunction in an In Vitro Model of Parkinson’s Disease

Antioxidants

Elisabetta Benedetti¹  Mariano Catanesi¹  Annamaria Cimini¹  Vanessa Castelli¹  Michele d’Angelo¹  Maria Grazia Tupone¹  Margherita Alfonsetti¹  Laura Brandolini²  Marcello Allegretti²  Daniela Iaconis²  Maddalena Fratelli³  Enrico Cabri³ 

[1] Department of Life, Health and Environmental Sciences, University of L’Aquila, 67100 L’Aquila, Italy;Dompé Farmaceutici SpA, Via Campo di Pile, 67100 L’Aquila, Italy;Pharmacogenomics Unit, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, 20156 Milan, Italy;

关键词: nutraceuticals;    neurodegeneration;    oxidative stress;    mitochondria;    brain;    reactive oxidative species;   

DOI  :  10.3390/antiox10091467

来源: DOAJ

【 摘 要 】

Methionine is an aliphatic, sulfur-containing, essential amino acid that has been demonstrated to have crucial roles in metabolism, innate immunity, and activation of endogenous antioxidant enzymes, including methionine sulfoxide reductase A/B and the biosynthesis of glutathione to counteract oxidative stress. Still, methionine restriction avoids altered methionine/transmethylation metabolism, thus reducing DNA damage and possibly avoiding neurodegenerative processes. In this study, we wanted to study the preventive effects of methionine in counteracting 6-hydroxydopamine (6-OHDA)-induced injury. In particular, we analyzed the protective effects of the amino acid L-methionine in an in vitro model of Parkinson’s disease and dissected the underlying mechanisms compared to the known antioxidant taurine to gain insights into the potential of methionine treatment in slowing the progression of the disease by maintaining mitochondrial functionality. In addition, to ascribe the effects of methionine on mitochondria and oxidative stress, methionine sulfoxide was used in place of methionine. The data obtained suggested that an L-methionine-enriched diet could be beneficial during aging to protect neurons from oxidative imbalance and mitochondrial dysfunction, thus preventing the progression of neurodegenerative processes.

【 授权许可】

Unknown