HO-1 induction attenuates renal damage and oxidative stress induced by K2Cr2O7

Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme; its inducible isozyme HO-1 protects against some types of acute tissue injury. The expression and functional role of HO-1 in rats with renal injury induced by potassium dichromate (K2Cr2O7) was investigated in this work. Rats were studied 24 h after a single injection of K2Cr2O7. To address the possible protective effect of HO-1 in this experimental model, this enzyme was induced by an injection of stannous chloride (SnCl2) 12 h before K2Cr2O7 administration. The functional role of HO-1 in K2Cr2O7 + SnCl2-treated animals was tested by inhibiting HO activity with an injection of zinc (II) protoporphyrin IX (ZnPP) 18 h before K2Cr2O7. In K2Cr2O7-treated rats: (i) renal HO-1 content, measured by Western blot, increased 2.6-fold; and, (ii) renal nitrotyrosine and protein carbonyl content, markers of oxidative stress, increased 3.5- and 1.36-fold, respectively. Renal damage and oxidative stress were ameliorated and HO-1 content was increased in the K2Cr2O7 + SnCl2 group. The attenuation of renal injury and oxidative stress was lost by the inhibition of HO activity in K2Cr2O7 + SnCl2 + ZnPP-treated animals. Our data suggest that HO-1 overexpression induced by SnCl2 is responsible for the attenuation of renal damage and oxidative stress induced by K2Cr2O7.