HEPATOTOXIC EFFECT OF NICKEL SULPHATE ON MICE

Background and Objective: Nickel is an important alloying element in metallic implants used in dentistry as well as in orthopedic surgery. The objective of this study was to see the effect of nickel sulphate on mice liver and to observe if there was any reversibility of pathological changes after cessation of nickel sulphate. Methods: Sixty male adult mice were randomly divided into three groups (n = 20). These groups were further subdivided (n = 10) into C1, C2 (Receive 0.25 ml sterile distilled water intraperitoneally) A1, A2 received 1 mg/kg nickel sulphate (high dose) intraperitoneally for 14 days. The animals from group C1 and A1 were sacrificed on day 15th. Liver was examined for gross, chemical and histopathological changes. After 14 day the injections of normal saline and nickel sulphate were stopped and animals were sacrificed at day 30th. Liver was removed and gross, chemical and histopathological changes were observed to see any reversibility of histopathological changes. Group C2 Receive 0.25 ml sterile distilled water intraperitoneally. GroupB1, B2 received 0.5 mg/ml (low dose) nickel sulphate intraperitoneally as a single dose for 14 days. The animals of groupC1 and B1 were sacrificed at day 15th. Liver was removed and examined. At day 30ththe animals of C2 and B2 group were sacrificed and gross and histopathological changes were compared to see any reversible change as compared to day 15th. Results: There was a significant change in size and weight of liver. There was elevation of serum enzymes activities (ALT, AST and bilirubin) in both experimental groups at day 30th and it was irreversible. The swelling of hepatocytes was present in 70% of animals in experimental groups at 15th day. There was 10% increase in swelling of hepatocytes in group A2 and 10% decrease in swelling of hepatocytes in group B2 at 30th day. Acute hepatitis (ballooning degeneration) was present in 30% of mice liver in group A1 at 15th day and only 10% in group B2 at 30th day. Histological and gross findings were reversed 10% to 20% but biochemical parameters (ALT, AST and bilirubin) were not reversed after stoppage of nickel sulphate in both high and low dose groups. Conclusion: It was concluded that nickel toxicity in experimental groups resulted in alterations in hepatocytes as change in size, weight and colour of liver, necrosis and acute hepatitis. The biochemical analysis revealed significant increased ALT AST and bilirubin, which supported the histological findings that nickel sulphate, is hepatotoxic. ALT and AST activities were not reversed at 30th day. The pathological changes as size, weight of liver, focal necrosis, zonal necrosis and acute hepatitis were ten to twe-nty percent reversible in experimental groups at 30th day.