LC/MS characterization of rotenone induced cardiolipin oxidation in human lymphocytes: Implications for mitochondrial dysfunction associated with Parkinson's disease
Published Date:May 03 2013
Source:Mol Nutr Food Res. 57(8):1410-1422.
Pubmed Central ID:PMC3810210
Funding:ES020693/ES/NIEHS NIH HHS/United States
HL70755/HL/NHLBI NIH HHS/United States
OH008282/OH/NIOSH CDC HHS/United States
R01 ES020693/ES/NIEHS NIH HHS/United States
R01 HL070755/HL/NHLBI NIH HHS/United States
U19 AI068021/AI/NIAID NIH HHS/United States
U19AIO68021/PHS HHS/United States
Rotenone is a toxicant believed to contribute to the development of Parkinson's disease.
Methods and results
Using human peripheral blood lymphocytes we demonstrated that exposure to rotenone resulted in disruption of electron transport accompanied by the production of reactive oxygen species, development of apoptosis and elevation of peroxidase activity of mitochondria. Employing LC/MS based lipidomics/oxidative lipidomics we characterized molecular species of cardiolipin (CL) and its oxidation/hydrolysis products formed early in apoptosis and associated with the rotenone-induced mitochondrial dysfunction.
The major oxidized CL species - tetra-linoleoyl-CL – underwent oxidation to yield epoxy-C18:2 and dihydroxy-C18:2 derivatives predominantly localized in sn-1 and sn-2 positions, respectively. In addition, accumulation of mono-lyso-CL species and oxygenated free C18:2 were detected in rotenone-treated lymphocytes. These oxidation/hydrolysis products may be useful for the development of new biomarkers of mitochondrial dysfunction.
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