Selenium Abrogates Tenofovir/Lamivudine/Efavirenz-Induced Hepatotoxicity in Rats

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Background: The therapeutic benefit of tenofovir/lamivudine/efavirenz (TLE) in the treatment of human immunodeficiency virus can be truncated by the occurrence of hepatotoxicity. This study evaluated the protective effect of selenium (Se) against hepatotoxicity induced by TLE in albino rats. Materials and Methods: Adult male albino rats (n = 40) randomized into four groups (n = 10) were used. Group 1 (Control) orally received normal saline (0.2 mL) daily. Group 2 orally received Se (0.1 mg/kg) daily. Group 3 orally received TLE (8.6/8.6/17.1 mg/kg) daily. Group 4 orally received Se (0.1 mg/kg) and TLE (8.6/8.6/17.1 mg/kg) daily. All rats were treated for 90 days. After treatment, the rats were euthanized, and serum samples were centrifuged from blood samples and assessed for liver function markers. Liver samples were harvested and evaluated for morphological changes and biochemical parameters. Results: Impaired liver redox status in TLE-treated rats was characterized by remarkable (P < 0.001) decreases in glutathione peroxidase superoxide dismutase, catalase, and glutathione levels with remarkable (P < 0.001) increases in malondialdehyde levels when compared to control. The alterations in liver function markers were marked by remarkable (P < 0.001) increases in serum aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyl transferase, conjugated bilirubin and total bilirubin levels when compared to control. Hepatocyte necrosis and fatty change were observed in TLE-treated rats. However, TLE-induced hepatotoxic changes were significantly (P < 0.01) reversed in Se supplemented rats when compared to TLE. Conclusion: Se may be clinically effective against hepatotoxicity caused by TLE.