Thymoquinone ameliorates renal oxidative damage and proliferative response induced by mercuric chloride in rats.

We tested the hypothesis if thymoquinone (2-isopropyl-5-methyl-1,4-benzoquinone) could ameliorate renal oxidative damage and proliferative response induced by mercuric chloride (HgCl2) in rats. HgCl2 (3 mg/kg) was administered subcutaneously to each one of two groups of rats: (i) HgCl2-thymoquinone group that received thymoquinone (10 mg/kg/day); and (ii) HgCl2 group that received vehicle instead of thymoquinone. A third group of rats was reserved as control group. Rats were killed 24, 48 and 72 hr after HgCl2 administration for histological and biochemical studies. Our findings show that treatment with thymoquinone offers imperative protection from HgCl2-induced nephrotoxicity. The deterioration of antioxidant enzymes, increment of serum creatinine and histological damage caused by HgCl2 are markedly improved by thymoquinone treatment. Apoptosis and proliferative reactions are also reduced. The maximal protection offered by thymoquinone treatment was particularly noticeable 48 and 72 hr after administration of the toxic agent at the time when histological damage, renal cell apoptosis and proliferative reactions reached their maximum. These observations may be attributed partially to the antioxidant effect of thymoquinone and suggest that it may be a clinically valuable agent in the prevention of acute renal failure caused by inorganic mercury intoxication.