Objective: Ischemia/Reperfusion (IR) injury is an important cause of acute kidney injury (AKI) in native and transplanted kidneys. This condition aggravates tissue damage by initiating an oxidative status. This study evaluates the effect of acute short-term selenium (Se) treatment on oxidative status and acute kidney injury.

Material and Methods: A total of 18 adult male Long Evans rats were randomly allocated into three groups. Under general anaesthesia and sterile conditions, the anterior abdominal wall was incised, and bilateral renal vessels were separated. Left renal artery was clamped, right nephrectomy was performed after 45 min of ischemia, left renal artery was de-clamped, and 4 hours reperfusion was performed. In IR and Se treated group, 0.625 mg/kg Se was administered orally 4 hours before the surgical procedure and 4 hours after the reperfusion period. In the IR group, one cc sterile saline was given orally with a similar protocol. All rats except the sham group were sacrificed after 4 hours following the second dose of saline and Se administration. Blood samples and kidney saved for histopathological investigation and creatinine, total thiol, native thiol, disulfides levels and dynamic thiol/disulfide ratio determinations.

Results: While there was no significant decrease in thiol levels before and after IR injury in the Se treated group, a significant decrease was observed in the IR group (p=0.345, p=0.028). There was no statistically significant improvement when the groups were compared in terms of renal functions and histopathological evaluation (p=0.053).

Conclusion: Our study revealed that acute short-term Se treatment improves the kidney redox status. However, histopathological changes in kidney and plasma creatinine levels remain unaffected. Moreover, Se administration increases the existing kidney damage after the injury has occurred.

Keywords: Ischemia-reperfusion injury, Selenium, Oxidative stress, Acute kidney injury, Salvage therapy