Biochemical and histological anomalies in the rat hepatic tissue following administration of bichromate and nickel in ionized form

Administration of bichromate ions at a dose of 60 mg/kg body wt to female rats, reduced dramatically both hepatic microsomal cytochrome P-450 content and the monooxygenase activities assayed, namely: N-demethylation of aminopyrine and O-demethylation of p-nitroanisole. At the same dose the bichromate ion treatment caused a substantial decrease in cytochrome b₅ content, but there was no significant reduction in NADPH-cytochrome c reductase activity. Administration of phenobarbital to bichromate ion pretreated rats did not induce a significant increase in cytochrome P-450 content nor in aminopyrine N-demethylase activity. Administration of nickel ions at a dose of 60 mg/kg body wt to female rats did not reduce to a significant level the content or the activity of any of the hepatic microsomal enzymes mentioned above, but did interfere in the de novo synthesis of cytochrome P-450 following phenobarbital treatment. The concentrations of nickel residues in the hepatic tissue of treated rats were only 5.8 times higher compared to the control rats, while those of chromium were 42 times higher than in control rats. Histological changes associated with the increase of bichromate concentration in treated rats were the formation of necrotic areas in the hepatic tissue and partial disintegration of the glomeruli and tubules in the kidney.