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Overexpression of manganese superoxide dismutase in mouse liver leads to defects in oxidative phosphorylation
Author(s) -
Steyl Samantha
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.634.5
Subject(s) - sod2 , superoxide dismutase , reactive oxygen species , antioxidant , chemistry , oxidative phosphorylation , biochemistry , hydrogen peroxide , superoxide , oxidative stress , dismutase , pharmacology , biology , enzyme
Non‐alcoholic fatty liver disease (NAFLD) is a chronic disease that is characterized by inflammation in the liver. This inflammation is due primarily to an increase in reactive oxygen species, and therefore antioxidant therapy can reduce the severity of the disease. However, these antioxidants have also been met with negative side effects, which warrants further investigation. Manganese superoxide dismutase, or MnSOD, is a mitochondrial antioxidant enzyme that converts then reduces superoxide levels by converting them into hydrogen peroxide. Hydrogen peroxide is then detoxified by a number of mitochondrial antioxidant enzymes. Although genetic overexpression of SOD2 could be beneficial to the treatment of NAFLD, preliminary data has shown that mice with SOD2 overexpression actually demonstrate defects in oxidative phosphorylation. These defects include reductions in levels of complex II and V measured by blue native PAGE, and reductions in levels of complex II, III and IV measured by SDS‐PAGE. Western blot results for reduction in levels of complex I, II, and III are under investigation. These data indicate that antioxidant therapy may have unexpected complications that should be considered before administration of these drugs.