Oral Selenium Supplementation Ameliorated Khat-Induced Hematotoxicity, Hepatotoxicity and Nephrotoxicity in a Mouse Model

Khat abuse in Kenya by young people is rapidly rising despite the much-publicized toxicological effects of khat. Furthermore, little research has focused on mediation strategies against khat-induced toxicities. Chemicals present in khat have been associated with multiple forms of toxicities. This study investigated the impact of khat on physiological and biochemical parameters and the putative role of selenium, a powerful antioxidant in mitigating khat-induced toxicities. Twenty-four, four weeks old male Balb/c mice were randomly divided into four groups, n=6. The first group was the control; groups two, four and three received 1500 mg/kg of khat or 200 mg/kg of selenium or both respectively. Exposure to khat resulted in increased relative organ weight of the spleen and brain; the liver, and kidney were unaffected. Khat-induced leukopenia was normalized in the presence of selenium. In addition, selenium treatment attenuated Khat-induced derangement of the WBC subtypes; neutrophils, monocytes and basophils. Khat-induced anemia was noted as depicted by decreased levels of RBCs, HGB and HCT when mice were exposed to khat. Importantly, selenium ameliorated the khat-driven anemia. Besides, khat administration led to increased serum levels of blood urea nitrogen and creatinine suggesting impaired renal function of excreting the metabolites; a phenomenon that was reversed in the presence of selenium. Furthermore, selenium assuaged khat-driven elevation of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT,) total bilirubin and alkaline phosphatase (ALP). The findings for the first time indicated that selenium administration prevented the khat-induced alterations in relative organ weights, stabilized hematological parameters, and normalized livers and kidney function markers. Keywords: Selenium; Khat; hepatotoxicity; hematotoxicity; nephrotoxicity