Selenium Protects against Tenofovir/Lamivudine/Efavirenz-Induced Nephrotoxicity in Rats

Abstract

Context: Tenofovir/lamivudine/efavirenz (TLE) used for the treatment of human immunodeficiency virus may cause acute or chronic nephrotoxicity. Aim: This study assessed the ability of selenium (Se) to prevent TLE-induced nephrotoxicity in albino rats. Materials and Methods: Forty healthy male albino rats (200–250) randomized into four groups (n = 10) were used. Group 1 (Control) was orally treated with normal saline (0.2 mL) daily for 90 days. Group 2 was orally treated with Se (0.1 mg/kg) daily for 90 days. Group 3 was orally treated with TLE (8.6/8.6/17.1 mg/kg) daily for 90 days. Group 4 was orally co-treated with Se (0.1 mg/kg) and TLE (8.6/8.6/17.1 mg/kg) daily for 90 days. After treatment, the rats were anesthetized and blood samples were collected and evaluated for serum renal function markers. Kidneys were examined for histology and oxidative stress indices. Results: Kidney oxidative damage in TLE-treated rats were marked by significant (P < 0.001) decreases in glutathione (GSH), GSH peroxidase, superoxide dismutase, and catalase levels with significant (P < 0.001) increases in kidney malondialdehyde levels when compared to control. Altered serum renal biochemical markers in TLE-treated rats were characterized by significant (P < 0.001) increases in creatinine, uric acid, and urea levels with significant (P < 0.001) decreases in total protein, albumin, bicarbonate, sodium, chloride, and potassium levels when compared to control. Tubular necrosis, lipid accumulation, and mesangial proliferation were observed in the kidneys of TLE-treated rats. TLE-induced nephrotoxicity was significantly (P < 0.01) reversed in Se supplemented rats when compared to TLE. Conclusion: Se may be clinically used for TLE-associated nephrotoxicity.