The current study was designed to evaluate the hepatoprotective role of
zinc after lead (Pb) treatment of
protein-deficient (PD) rats. The animals were subjected to seven different treatment groups: G-1 (normal control, 18%
protein), G-2 (
protein-deficient, 8%
protein), G-3 (Pb-treated, 100 mg/kg
body weight of
lead acetate), G-4 (Zn-treated,
zinc sulfate at a dose level of 227 mg/L
drinking water), G-5 (PD + Pb-treated), G-6 (PD + Zn-treated), and G-7 (PD + Pb + Zn-treated).
Serum albumin levels and total
serum protein contents were estimated to assess the severity of
protein deficiency at the end of 8 weeks in all the treatment groups. Also, the study explored the role of
zinc on antioxidative defense system
enzymes in liver of
protein-deficient rats subjected to lead toxicity treatment. Further, the study was extended to elucidate the levels of
zinc and lead in liver tissue after different treatments of rats using positron-induced X-ray emission technique (PIXE). The current study indicated a significant change in the levels of various antioxidative
enzymes and
serum albumin as well as total
protein contents of
protein-deficient rats subjected to lead treatment. A significant increase in the levels of
malondialdehyde (MDA),
catalase, and
glutathione peroxidase (GPx) was seen after 8 weeks of lead treatment of
protein-deficient rats. On the contrary, levels of
albumin, total
protein content,
superoxide dismutase (SOD), GSH, were found to be decreased. Interestingly,
zinc supplementation has tended to normalize the altered levels of these
enzymes to a significant extent. The levels of
zinc in liver tissue was found to be decreased significantly in
protein-deficient as well as lead-treated rats. However, hepatic
zinc concentration was increased to a significant extent in
protein-deficient rats supplemented with
zinc when compared with
protein-deficient rats. Further, the presence of lead was also observed in livers of lead-treated animals. In conclusion, the study revealed the antioxidative role of
zinc in hepatotoxic conditions induced by subjecting the rats to
protein-deficient diet and lead treatment.