Thesis Type: Doctorate
Institution Of The Thesis: Gazi University, Fen Bilimleri Enstitüsü, Turkey
Approval Date: 2014
Thesis Language: Turkish
Student: Hatice Baş
Supervisor: YUSUF KALENDER
Open Archive Collection: AVESIS Open Access Collection
Abstract:For many years lead has been recognized as a highly toxic metal to both humans and animals. The aim of this study is to investigate the effects of lead nitrate on diabetic and non-diabetic rat kidney tissues and the protective role of sodium selenite which is known to have antioxidant property. In the present study, lead nitrate (22,5 mg/kg/day) and sodium selenite (1 mg/kg/day) were given to male rats through gavage. After 28 days, in lead nitrate and sodium selenite+lead nitrate groups we observed increment in serum urea, uric acid, creatinin and kidney MDA levels, also decreasing in antioxidant enzyme activities, body and kidney weights compared with control. In sodium selenite+lead nitrate group, we observed the protective effect of sodium selenite on examining parameters compared with lead nitrate group. Similar results were observed in diabetic groups. When we compared control with diabetic control, sodium selenite with diabetic sodium selenite, lead nitrate with diabetic lead nitrate and sodium selenite+lead nitrate with diabetic sodium selenite+lead nitrate groups we determined increment in kidney weights, serum urea, uric acid, creatinin and kidney MDA levels, also we determined decreasing in antioxidant enzyme activities and body weights in diabetic groups. Severe histopathological changes were observed in the lead nitrate treated rats, mild histopathological changes were observed in sodium selenite+lead nitrate treated animals. In diabetic vii groups we also observed histopathologic differences but there were no protective effect of sodium selenite against these changes. As a result, lead nitrate caused nephrotoxicity and sodium selenite alleviated lead nitrate induced toxicity in rat kidneys but sodium selenite didn't protect kidneys against diabetes mediated toxicity.