Alteration of lipid peroxidation and mitochondrial viability in CCL4 - induced liver injury

Alteration of lipid peroxidation and mitochondrial viability in CCL4 - induced liver injury

Carbon tetrachloride (CCl4) is a well-known environmental biohazard. It is particularly toxic to the liver, where it causes hepatocellular degeneration, centrilobular necrosis and impairs different enzymatic systems. The generation of free radicals appears to be pivotal in CCl4 hepatotoxicity: CCl4 is metabolized by cytochrome P-450 to produce the trichloromethyl radical, which initiates a cascade of free radical reactions resulting in an increase of lipid peroxidation and a reduction in some enzyme activities. 10 male rats were equally divided in to 2 groups (05 rats each). Group I (control), while Group II was given CCl4 (0.2 ml/kg /day) once daily for two weeks. After treatment liver mitochondria was isolated. The lipid peroxidation (LPO) concentration and mitochondrial toxicity were measured. Oxidative stress induced with CCl4 in liver mitochondria was evident by a significant increase in LPO and reduce viability of liver mitochondria. It is concluded that oxidative damage is the mechanism of CCL4 toxicity in the mitochondria that can be damaged some organs especially liver