JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2008, Vol. 46 ›› Issue (12): 1192-1196.
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LI Di, SUN Lihong, SUN Jie, YAN Li, QU Bin
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Objective To explore the effect of clofibrate on freshly isolated mouse liver mitochondria and a cultured hepatocyte cell line, AML-12. Methods Mitochondrial membrane potential was determined by using the fluorescent dye, JC-1. Levels of reactive oxygen species were measured with the fluorescent probes DCFDA. CsA and antioxidants such as Vitamin C, deferoxamine and catalase were used to protect cells. Results Application of clofibrate at concentrations greater than 0.3mmol/L rapidly collapsed the ΔΨm both in liver cells and in isolated mitochondria. The loss of ΔΨm occurred prior to cell death, as revealed by the protective effect of cyclosporin A (CsA) on the decrease in ΔΨm. Treatment of hepatocytes with clofibrate caused a significant increase in intracellular and mitochondrial ROS. Antioxidants such as Vitamin C, deferoxamine, and catalase were able to protect cells against lofibrate-induced loss of viability. Conclusion Clofibrate may impair mitochondrial function, stimulates formation of ROS, and eventually contributes to cell death.
Key words: Clofibrate; Mitochondrial membrane potential; Apoptosis; Free radicals
LI Di, SUN Lihong, SUN Jie, YAN Li, QU Bin. Clofibrate induced hepatotoxicity by mitochondrial damage[J].JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2008, 46(12): 1192-1196.
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