Evidence for renal ischaemia as a cause of mercuric chloride nephrotoxicity.

The present study was undertaken to investigate if the source of oxidative stress and the renal injury produced by mercuric chloride could be renal ischaemia. Verapamil Vp was used because it was described that calcium channel blockers protect cells from nephrotoxicants and from ischaemia. Vp (75 micrograms/kg, i.v.; 30 min before HgCl2 injection) prevented mercuric chloride renal injury observed 1 h post-HgCl2 injection as measured by clearance techniques. Vp also prevented the diminution of non-protein-sulfhydryls (NPSH) and the increased lipid peroxidation (LPO) induced by HgCl2 in renal tissue. Hg2+ toxicokinetic alterations were not observed in Vp plus HgCl2 treated rats, nor was Vp ability found as a free radical scavenger in renal tissue homogenates. The results described in this study give some evidence for the role of renal ischaemia in the production of oxidative stress, generating LPO and functional and morphological renal injury described in mercuric chloride treated rats.