Tin chloride pretreatment prevents renal injury in rats with ischemic acute renal failure

Abstract

These findings indicate that tin chloride pretreatment significantly ameliorates renal injury in rats with IARF by virtue of its specific heme oxygenase-1 induction in renal epithelial cells. These findings also suggest that heme oxygenase-1 induction plays an important role in protecting renal cells from oxidative damage caused by heme.

Fundamental Role of Heme Oxygenase in the Protection Against Ischemic Acute Renal Failure

“…In contrast to Sn-PP or Sn-MP, tin chloride (SnCl2) treatment has been shown to potently induce HO-1, which is almost entirely restricted to the kidney (18). We examined the effect of SnCl2 or Sn-MP in the kidney in rats with IARF as well as their effects on renal function as determined by morphological examination and by measurements of serum creatinine concentrations (16,19). We have in fact confirmed a transient but strong induction of HO-1 mRNA in the kidney of rats following ischemia / reperfusion (16).…”

“…1) (19). In contrast, inhibition of HO activity by the administration of Sn-MP to SnCl2-pretreated animals abolished the beneficial effect of the SnCl2 pretreatment on ischemic renal dysfunction, indicating the fundamental protective role of HO-1 in the renal epithelial cells against oxidative stresses (19).…”

“…Tin pretreatment also significantly attenuated the severity of ischemic renal injury. In contrast, when SnCl2-treated animals were treated with Sn-MP, microsomal heme concentrations were elevated and resulted in an aggravation of renal function (19). Thus, HO-1 induced by SnCl2 pretreatment effectively decreased the excess amount of toxic "free heme", resulting in the amelioration of the ischemic renal injury.…”

“…This result indicates that HO-1 mRNA is induced by SnCl2 treatment in a highly kidney-specific manner (19). Following SnCl2 treatment, a marked elevation of renal HO-1 mRNA was observed, followed by increases in HO-1 protein expression and HO activity (19).…”

Elucidating the Role of Biliverdin Reductase in the Expression of Heme Oxygenase-1 as a Cytoprotective Response to Stress

“…In vivo studies also demonstrated the ability of HO-1 induction to protect against acute renal failure in rats following ischemia/reperfusion (Toda et al, 2002) and exposure to mercuric chloride (Yoneya et al, 2000). Ischemia/reperfusion involves exposing the tissue to a sequence of oxygen deprivation followed by reoxygenation.…”