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Oxidized low-density lipoprotein and 15-deoxy-^12,14-PGJ₂ increase mitochondrial complex I activity in endothelial cells

¹Department of Pathology and ²Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294

Submitted 2 June 2003 ; accepted in final form 21 July 2003

Oxidized lipids are capable of initiating diverse cellular responses through both receptor-mediated mechanisms and direct posttranslational modification of proteins. Typically, exposure of cells to low concentrations of oxidized lipids induces cytoprotective pathways, whereas high concentrations result in apoptosis. Interestingly, mitochondria can contribute to processes that result in either cytoprotection or cell death. The role of antioxidant defenses such as glutathione in adaptation to stress has been established, but the potential interaction with mitochondrial function is unknown and is examined in this article. Human umbilical vein endothelial cells (HUVEC) were exposed to oxidized LDL (oxLDL) or the electrophilic cyclopentenone 15-deoxy-^12,14-PGJ₂ (15d-PGJ₂). We demonstrate that complex I activity, but not citrate synthase or cytochrome-c oxidase, is significantly induced by oxLDL and 15d-PGJ₂. The mechanism is not clear at present but is independent of the induction of GSH, peroxisome proliferator-activated receptor (PPAR)-, and PPAR-. This response is dependent on the induction of oxidative stress in the cells because it can be prevented by nitric oxide, probucol, and the SOD mimetic manganese(III) tetrakis(4-benzoic acid) porphyrin chloride. This increased complex I activity appears to contribute to protection against apoptosis induced by 4-hydroxynonenal.

oxidized lipid; reactive oxygen and nitrogen species; peroxisome proliferator-activated receptors; 4-hydroxynonenal

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