Efficacy of vitamin e to reduce some heavy metals toxicity in albino rats

Ninety albino rats were used to evaluate the ability of vitamin E to minimize or prevent the adverse effects of mercuric chloride and lead acetate. They were randomly assigned to 6 groups: intragastrically administered saline (gp. 1), twice weekly 4.6 mg of mercuric chloride / kg. B. wt. (gp. 2), daily 15 mg of lead acetate / kg. B. wt. (gp.3), 200 mg of vitamin E / kg. B. wt. diet (gp. 4), 200 mg of vitamin E / kg. B. wt. diet + 4.6 mg of mercuric chloride / kg. B. wt. (gp. 5) and 200 mg of vitamin E / kg. B. wt. diet + 15 mg of lead acetate / kg. B. wt. (gp. 6). Five rats of each groups were sacrificed 1,3 and 5 months post administration (PA), necropsied and specimens from the kidneys, liver, brain and spleen were collected for pathological examination beside blood samples for hematological and biochemical estimation. Long-term exposure of mercuric chloride revealed nephrotoxicosis manifested by significant increase of BUN and serum cretonne, proliferation of the endothelial lining of the glomerular tufts and thickening of the Bowman’s capsule, with degenerative and necrotic changes beside hepatotoxicosis accompanied with significant increase of GGT, AST, ALT, ALP beside significant decrease of serum total protein, albumin and globulin, in addition to brain damage. Meanwhile, the chronic exposure to the lead acetate induced hepatorenal damage with the presence of eosinophilic intranuclear bodies in the renal and hepatic cells. Anemia, macrocytic hypochromic with mercury and normocytic normochromic with lead, leucopenia and lymphopenia were observed by hematological examination during the course of the experiment. These lesions were alleviated or completely absent in vitamin E-treated groups (5 and 6).