Carbon Tetrachloride May Alter The Hepatic Contents Of Antioxidants

Chronic CCl4 administration is known to induce cell necrosis by increased oxidative stress,46 and repeated injections of CCl4 initiate the fibrogenic process in the liver and may result in cirrhosis.47 Administration of vitamin E prevents CCl4-induced liver necrosis and cirrhosis, which supports the role of reactive oxygen species in liver damage associated with CCl4.48 CCl4 is metabolically activated by cytochrome P450 to form ^CCl3 free radicals, which initiate lipid peroxidation in the cell and decrease cellular ubiquinol-10.49 Kishi et al. demonstrated that administration of ubiquinone supplement attenuated CCl4-induced cell necrosis.49 In a study in which rats were exposed to diethylnitrosamine (DEN) as initiator, followed by repeated injections of carbon tetrachloride (CCl4)

| Serum activities of ALT (U/l) | | Hepatic contents of ubiquinol (nmol/100 g)

FIGURE 23.2 Serum alanine aminotransferase activities (ALT) and hepatic contents of ubiquinol (reduced ubiquinone-9) in male Wistar rats exposed to dietary carbonyl iron with or without chronic ethanol administration. Animals receiving iron + ethanol demonstrated significantly increased ALT activities in serum compared with the other groups (* = p < 0.01). Hepatic contents of ubiquinol were significantly decreased in animals receiving ethanol alone, compared with controls (# = p < 0.05), whereas treatment with iron plus ethanol led to significantly decreased levels compared with all other groups (* = p < 0.05). (Data from [38]).

0 0

Post a comment