Acrolein-Induced Toxicity—Defective Mitochondrial Function as a Possible Mechanism
Administration of acrolein (2.5 mg/kg body weight/day) to rats for 45 days depleted the glutathione level in liver, which triggered an imbalance in the antioxidant defense, resulting in lipid peroxidation. Enhanced lipid peroxidation damaged the membranous structure of mitochondria, which was indicated by the loss of lamellae, and increased the oxidation of exogenously added NADH. Loss in membrane integrity altered the activities of the tricarboxylic acid cycle enzymes and levels of cytochromes. Decreased rate of ADP—stimulated oxygen uptake, respiratory coupling ratio, and ATP synthesis—were also observed. We report that the acrolein-induced toxicity is mediated through the depletion of GSH leading to impairment of rat liver mitochondrial function.
KeywordsGlutathione Lipid Peroxidation NADH Oxygen Uptake Antioxidant Defense
Unable to display preview. Download preview PDF.