Abstract

We have shown that the ameliorative effect of stannous chloride (SnCl 2) pretreatment on potassium dichromate (K 2Cr 2O 7)-induced renal damage 24 h after K 2Cr 2O 7 injection was associated with the induction of heme oxygenase-1 (HO-1). In this work we evaluated: (a) if the protective effect of SnCl 2 (given 12 h before K 2Cr 2O 7) is associated with changes in the renal activity of HO-1, superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) 24 and 48 h after K 2Cr 2O 7 injection, and (b) if HO-1 induction is indispensable before K 2Cr 2O 7 injection. It was found that the protective effect of SnCl 2 on renal function was observed both at 24 and 48 h reaching its maximum at 24 h when HO-1 expression was higher. Cu,Zn-SOD, Mn-SOD, and GR activities remained unchanged whereas GPx and CAT activities decreased at 48 h in K 2Cr 2O 7-treated rats. The activity of Cu,Zn-SOD, Mn-SOD, GPx, CAT, and GR was unchanged in the SnCl 2-treated rats. To fulfill the objective (b) groups of rats treated with K 2Cr 2O 7 and SnCl 2 (given at the same time or 12 h after K 2Cr 2O 7) were studied 24 h after K 2Cr 2O 7-injection. The simultaneous injections of SnCl 2 and K 2Cr 2O 7 had no protective effect whereas the injection of SnCl 2 12 h after K 2Cr 2O 7 exacerbated renal damage. In conclusion, the protective effect of SnCl 2 on K 2Cr 2O 7-induced nephrotoxicity is associated with HO-1 induction and not with other antioxidant enzymes (Cu,Zn-SOD, Mn-SOD, GPx, GR, and CAT) and SnCl 2 has a preventive and not a therapeutic effect on renal damage induced by K 2Cr 2O 7.

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