The role of sodium selenite in protection of primary hepatocytes and liver against carbon tetrachloride toxicity in grass carp

Abstract

The effect of different concentrations of carbon tetrachloride (CCl-4) was studied in the primary culture of grass carp hepatocytes. As the concentration of 10 mu-l/3 times 10-6 cells CCl-4, the increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) as well as lactate dehydrogenase (LDH) released all from the hepatocytes was observed, and so was the increase of the percentage of damaged cells. The adding of sodium selenite (0.2 mu-g/ml) to RPMI-1640 liquid medium and cultured hepatocytes reduced the release of ALT, AST, LDH and the extent of the cell damage. In another experiment evaluating the effect of sodium selenite and CCl-4, grass carp fingerlings were injected intraperitoneally with Na-2SeO-3 0.1mg/kg.bw each day for three consecutive days, and then with 1ml/kg.Bw CCl-4. Twenty-four hours later, the relative activity of hepatic superoxide dismutase (SOD) was found to rise 91.5% higher in these fingerlings than those injected with CCl-4 only. Seven days later it was still 54.5% higher. The level of serum ALT decreased gradually. The activity level of hepatic lipid peroxide decreased significantly (P lt 0.05) and that of P-450 increased significantly (P lt 0.01) and so did the contained hepatic microsomal protein (P lt 0.05) in those fingerlings injected with selenium and then CCl-4. Light microscopic observations revealed a decrease of hepatic damage and an increase of nuclear numbers, suggesting that cell divisions might have taken place. It is indicated that sodium selenite may elevate the capacity of hepatic SOD in scavenging free radicals, and hepatic counteractions on CCl-4 toxicity