Renal function and oxidative stress following gentamicin induced renal injury in rats treated with erythropoietin, iron and vitamine E

Abstract

Effects of erythropoietin, iron, and vitamin E on renal function and oxidative stress induced by gentamicin in rats were investigated. Rats were divided into 5 groups; group 1 (control: NSS injection on day 1-12); group 2 gentamicin injection ( 100 mg/kg s.c. on day 5-12 ); group 3 gentamicin plus erythropoietin (EPO) (gentamicin 100 mg/kg s.c., EPO 100 i.u./kg s.c. on day 5-12) group 4 gentamicin plus EPO and iron (iron 500 mg/kg i.p. on day 4, gentamicin 100 mg/kg, EPO 100 i.u./kg s.c. on day 5-12 and) ; group 5 gentamicin plus EPO, iron, and vitamin E (vitamin E 250 i.u./kg orally on day 1-3, iron 500 mg/kg i.p. on day 4, gentamicin 100 mg/kg, EPO 100 i.u./kg s.c. iron 500 mg/kg i.p., on day 5-12). The results showed that plasma creatinine and BUN concentrations of rats in group 2,3,4, and 5 were significantly increased while glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) decreased. The fractional excretion of Na+ and K+ and protein excretion were higher in groups 2,3,4 and 5. Group 3 with EPO did not improve GFR and ERPF. However, kidney GSH was decreased compared with group 2. Rats receiving iron showed no changes in renal function and oxidative stress compared with group 3. However, supplement with vitamin E in group 5 caused higher ERPF. In conclusion, gentamicin induced nephrotoxicity by causing severe damage of both glomerulus and renal tubular cells with alteration of oxidative stress. EPO and iron did not alter renal function but vitamin E supplementation could improve blood flow to the kidney.