Selenium Nephroprotection through Inhibition of PERKEIF2α- CHOP Pathway in Lead Intoxicated Male Rats

Document Type : Original Article

Authors

1 Crime Investigation Research Department, National Center for Social and Criminological Research, Cairo Egypt

2 Environmental Research Department, National Center for Social and Criminological Research, Cairo Egypt.

3 Pharmacology Department, Faculty of Medicine, Ain Shams University, Cairo Egypt.

Abstract

Background: Lead contamination has turned into a major concern as it serves no useful purpose in the human body. Its presence in the body can lead to toxic effects on different organs. Aim: The purpose of the present study is to examine the efficacy of selenium in mitigating leadinduced oxidative stress and kidney injury in male albino Wistar rats. Further to study the underlying molecular mechanism. Methods: We hypothesized that selenium protect against lead nephrotoxicity by testing various parameters of kidney function in male rats treated for 28 days with o.5 mg/kg selenium versus control male rats that received a vehicle. Results: The results showed an increase of serum urea, creatinine, uric acid and urinary albumin in rats intoxicated with lead compared to control group. The increase of these parameters would indicate renal toxicity which is confirmed by histopathological changes. Lead intoxicated rats had significant increment in apoptosis as well as phosphorylated PERK, eIF2α and apoptotic proteins as CHOP, caspase 3 and 8 in the kidneys, which were attenuated by selenium treatment. Conclusion: This study clearly demonstrated that activation of PERK- eIF2α -CHOP signaling pathway was involved in lead induced nephrotoxicity in rats and selenium inhibited lead nephrotoxicity partly through suppression of PERK- eIF2α CHOP pathway.

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