Deterioration of ischemia/reperfusion-induced acute renal failure in SOD1-deficient mice

Free Radic Res. 2007 Feb;41(2):200-7. doi: 10.1080/10715760601038791.

Abstract

Reactive oxygen species (ROS) are likely candidates for involvement in ischemia/reperfusion-induced acute renal failure (ARF). In this study, the issue of whether superoxide dismutase (SOD1)-deficiency exacerbates the ischemia/reperfusion-induced ARF was examined. At two weeks after a right nephrectomy of mice, the left renal vessels were clipped to induce renal ischemia and were then released after 45 min. The severe renal damage observed at one day was partially recovered at seven days after the induction of ischemia. SOD1-/- mice suffer from severe ARF compared with SOD1+ - and SOD1+/+ mice. The damage was more evident in aged animals (24-28 week old) than younger ones (10-12 week old). The expression of major antioxidative and redox enzymes, except for CuZnSOD, were substantially unchanged. Thus, the increased ARF in SOD1-/- mice appears to be mainly attributable to a deficiency in CuZnSOD. These data support the view that ROS are exacerbating factors in ischemia/reperfusion-induced ARF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / etiology*
  • Acute Kidney Injury / physiopathology
  • Age Factors
  • Animals
  • Blood Urea Nitrogen
  • Creatinine / blood
  • Ischemia / physiopathology*
  • Kidney / blood supply*
  • Mice
  • Mice, Knockout
  • Nephrectomy
  • Oxidation-Reduction
  • Oxidative Stress
  • Reactive Oxygen Species / toxicity*
  • Reperfusion Injury / physiopathology*
  • Superoxide Dismutase / deficiency*
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism
  • Superoxide Dismutase-1

Substances

  • Reactive Oxygen Species
  • Creatinine
  • Sod1 protein, mouse
  • Superoxide Dismutase
  • Superoxide Dismutase-1
  • superoxide dismutase 2