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Food Chem Toxicol. 2012 Aug;50(8):2729-35. doi: 10.1016/j.fct.2012.04.047. Epub 2012 May 17.

Protection of L-methionine against H₂O₂-induced oxidative damage in mitochondria.

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1
Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.

Abstract

Reactive oxygen species (ROS) is reported to be a critical pathogenic factor and mitochondria is one of the susceptible subcellular organs for oxidative damage. Methionine sulfoxide reductase A (MsrA) is a key anti-oxidant enzyme associated with cytoprotection and previous reports have revealed its importance in mitochondrial function. The anti-oxidation of MsrA is due to Met-centered redox cycle, suggesting that Met-centered redox cycle may play a critical role in mitochondrial protection. L-Methionine (L-Met), a natural amino acid with anti-oxidation activity, can mimic the effect of Met-centered redox cycle. Here, we investigated the protection of L-Met on H(2)O(2)-induced oxidative damage in mitochondria. Our study demonstrated that L-Met protected H(2)O(2)-induced injury in CHO cells. Cytoprotections of L-Met at low concentrations (1-5mM) were abolished by dimethyl sulfoxide (DMSO), a competitive inhibitor of MsrA function, suggesting that these effects may involve the participation of MsrA. Overexpression of MsrA in CHO cells protected mitochondria from H(2)O(2)-induced downtrend of membrane potential and production of mitochondrial superoxide. Pre-treatment with L-Met (1mM) produced a similar effect on the mitochondrial protection against H(2)O(2). Furthermore, it was observed that topical application of L-Met can prevent 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced oxidative damage in the skin of mice. These results suggest that anti-oxidation activity of L-Met may promise a new strategy for the prevention of oxidative stress-induced damage.

PMID:
22609493
DOI:
10.1016/j.fct.2012.04.047
[Indexed for MEDLINE]
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