Protective Effect of Zinc on Carbon Tetrachloride-Induced Liver Injury in Rats

Document Type

Article

Publication Date

1-1-1973

Description

In rats treated for 20 or 34 days with CCl4 (0.2 ml/100 g, ip, twice weekly) a significant increase in the content of malonaldehyde product in microsomal and mitochondrial fractions of the liver occurred. The raise in this indirect index of lipid peroxidation correlated with labilization of lysosomes, as evidenced by the increased portion of free β-glucuronidase present in the 15,000g supernatant of the liver homogenate. At the same time, the amount and the synthesis of collagen was significantly elevated. After zinc acetate administration (5 mg/100 g/day, intragastrically) to rats receiving CCl4, the content of malonaldehyde in the microsomal, as well as the mitochondrial fraction of the liver, was significantly lower. This correlated with a decreased portion of free β-glucuronidase and a decrease in the amount and in the rate of biosynthesis of collagen. Administration of zinc to normal rats had no effect on the amount and synthesis of collagen in the liver. The free and total activity of lysosomal β-glucuronidase in the liver was also unaltered by zinc in normal animals. The level of malonaldehyde was inhibited only in the microsomal fraction. In rats kept on a diet high in zinc (1000 ppm), the content of endogenously-, as well as exogenously-induced malonaldehyde in the liver was lower. Some factors influencing the content of malonaldehyde in intact rat liver are described. We believe that zinc protects the liver against the noxious effect of CCl4 primarily by interference with lipid-peroxidation-related tissue damage. Other possibilities of the protective effect of zinc administration in tissue injury have not been ruled out.

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