الفهرس | Only 14 pages are availabe for public view |
Abstract Tamoxifen (TAM) is a hormonal selective estrogen modulator used in the prevention and treatment of breast cancer. TAM-induced nonalcoholic fatty liver (NAFL) through lipid accumulation, liver steatosis and nephrotoxicity through oxidative stress and an alteration in the glutathione redox system. This study aimed to assess the complications of TAM on liver and kidney and the potential protective and therapeutic efficacy of sodium butyrate (NaBu) to reduce liver steatosis and nephrotoxicity induced by TAM in male rats. Animals were divided mainly into protective and therapeutic groups. The protective main group subdivided into: (control), (NaBu), (TAM) and (NaBu-TAM) subgroups. Therapeutic group subdivided into: (control), (NaBu), (TAM), and (TAM-NaBu) subgroups. Physiological studies were studied using liver function, lipid profile, oxidative stress, kidney function tests and histopathological examination. The results revealed that, NAFL was assessed in TAM group by increasing the levels of total lipids, triglycerides and MDA. In addition, to the reduction in some biochemical parameters and some oxidative biomarkers which have bad effects on liver and kidney functions. Sodium butyrate administration as a protective or therapeutic agent showed improvement in the liver and kidney function tests with an increase in the tested endogenous scavengers accompanied with healthy hepatic and renal histopathological examination. Sodium butyrate exhibited the protective and therapeutic roles in dissolving the lipid accumulation and reducing the steatosis and kidney damage generated by TAM |