Nickel, a potent toxic metal, is very harmful to the environment and to humans because of its in vivo accumulation in liver. The present study was conducted to investigate the protective effect of selenium (Se) against nickel toxicity on liver function in preimplanted Wistar albino rats. NiCl2 was given on day three of pregnancy either in distilled drinking water at a dose of 20 mg/L/day) for 16 consecutive days or as a single s.c. dose of 25, 50, or 100 mg/kg. Se was given as an s.c. injection (0.3 mg/kg) together with the higher dose (100 mg/kg) of NiCl2. Changes in plasma glucose, triglycerides and total cholesterol were measured in treated and control groups on days five and 20 of gestation. NiCl2 s.c. induced on day five of gestation showed a significant (<0.05) decrease in plasma triglycerides, with a dose of 100 mg / kg (-48 percent). This decrease was maintained at day 20 of gestation with doses of 50 mg / kg (-36 percent) and 100 mg / kg (-31 percent). In contrast, the low dose induced an increase of + 50 percent in plasma triglyceride compared to controls. In addition, NiCl2 s.c. caused on day five of gestation a significant decrease (p <0.05) in plasma total cholesterol with the low (-50 percent) and medium doses (-26 percent). However, the dose of 100 mg / kg induced a significant increase (114 percent) in plasma total cholesterol on day 20 of gestation compared to controls. NiCl2 s.c. induced a significant increase in plasma glucose (+125 percent) on day 20 of pregnancy. The pretreatment with Se counteracted the effects of NiCl2 on plasma glucose, total cholesterol and triglycerides.

NiCl2 administered in the drinking water induced a significant increase (<0.05) in plasma triglycerides (+68 percent) and cholesterol (+49 percent) on day 20 of gestation, while on day five of gestation NiCl2 s.c. induced a significant decrease in cholesterol (-31 percent) compared to controls. All doses of NiCl2 induced an alteration of liver architecture. Co-administration of Se with NiCl2 restored the structure of the liver.

These results suggested that selenium has a hepatoprotective role against the toxicity induced by NiCl2 administered subcutaneously in preimplanted rats.