Sodium Butyrate Attenuates Nephrotoxicity Induced by Tamoxifen in Rats

Article history: Received on: 15/04/2016 Revised on: 21/05/2016 Accepted on: 09/06/2016 Available online: 28/06/2016 Tamoxifen (TAM) is a hormonal selective estrogen modulator used in the prevention and treatment of breast cancer. It associated with increased in the oxidative stress in cells leading to tissue injury. Sodium butyrate (NaBu) increased the glutathione redox system and diminished the oxidative stress. The purpose of this study was to elucidate the ameliorative effect of NaBu against TAM-induced kidney injury by reducing the generation of oxidative stress. Rats were divided mainly into four group as follow: control, rats received saline for 14 days orally then saline intraperitoneally (i.p.) for 7 days, NaBu, rats received saline orally for 14 days, NaBu (300mg/kg) (i.p.) for 7 days, TAM, rats received TAM (40mg/kg) orally for 14 days, then saline (i.p.) for 7 days, (TAM-NaBu) rats received TAM orally for 14 days, NaBu (i.p.) for 7 days. Kidney injury followed by TAM treatment was assessed by the elevation in the levels of creatinine, urea, uric acid and MDA and reduction in some oxidative biomarkers, in addition to the abnormal architecture of the kidney. Conversely, Administration of sodium butyrate could ameliorate all of these damaging effects in the antioxidant system in the TAM-treated group. NaBu affords significant increments in the antioxidant enzymes. In addition, it has the therapeutic capacity to protect the kidney from the oxidative stress induced by TAM through improving the kidney function and diminishing the free radicals. Supplementation of NaBu could be useful in alleviating TAM-induced kidney injury.