Abstract
Introduction: Selenium (Se) is an antioxidant and reactive oxygen species (ROS) scavenger.
Objectives: This study was conducted to evaluate the effects of Se on renal functional parameters,
oxidative stress biomarkers, myeloperoxidase (MPO) activity, and the nitric oxide (NO) level in
renal ischemia-reperfusion (IR) injury in rats.
Materials and Methods: Twenty-four male Wistar rats (180–200 g) were selected and subsequently
divided into three groups (n=8); group 1 as the control group, group 2 as the untreated group (IR
without treatment) and group 3 as the IR group (treated with Se (1 mg/kg/d, intraperitoneally).
The period of Se administration was 2 weeks before the inducing renal IR. To cause renal IR, renal
pedicles were occluded by safe clamps for 45 minutes. Then, the clamps were removed and 24 hours
was considered as reperfusion. After the study, blood sampling from the hearts and the removal of
the left kidney was conducted immediately for biochemical measurements.
Results: Renal IR significantly increased serum levels of urea, creatinine (Cr), serum and renal
malondialdehyde (MDA) levels, serum NO level, and MPO activity. It significantly decreased serum
and renal glutathione (GSH) levels, serum paraoxonase 1 activity, serum and renal activities of
catalase (CAT), and glutathione peroxidase (GPx). Se could reverse these findings, but the increase
of paraoxonase 1 activity and the decrease of MPO activity in IR animals were not significant.
Conclusion: It seems that Se has protective effects on inflammatory indices. It can ameliorate renal
IR complications which are associated with oxidative stress and inflammation.