6 результати
Papillary necrosis was observed in the kidneys of rats, 72 h after receiving a single injection of bromoethylamine (BEA). This effect was associated with renal glutathione (GSH) depletion 1 h after the administration of BEA. Stimulation of renal GSH synthesis by pretreatment of the animals either
The effect of diphenylamine on renal cortical, outer medullary and inner medullary glutathione (GSH) concentrations and the effect of GSH depletion on the nephrotoxicity of diphenylamine were investigated in male Syrian hamsters. A dose-dependent decrease in renal cortical GSH was observed within 1
2-Bromoethanamine (BEA) causes renal papillary necrosis (RPN) in rats after a single dose and has been widely used as a model compound for studying the lesion. Although the metabolism of BEA may be an important determinant of toxicity, the metabolic fate of the compound has not been fully
N-phenylanthranilic acid is a chloride channel blocker that causes renal papillary necrosis in rats. Studies were conducted in two strains of male rats to evaluate novel biomarkers of nephrotoxicity. Han-Wistar rats were given daily oral doses of 50, 350, or up to 700 mg/kg/day of NPAA, and
Analgesic nephropathy is a unique drug-induced kidney disease characterized pathologically by renal papillary necrosis and chronic interstitial nephritis, and is the result of excessive consumption of combination antipyretic analgesics. The clinical features of the disorder relate mainly to the
BACKGROUND
The effect of bromoethylamine (BEA) administration on lipid peroxidation and on the activities of antioxidant enzymes was studied.
METHODS
Adult rats received BEA at 1.2 mmol/kg, a dose that produces renal papillary necrosis. Lipid peroxidation assessed by maximal rate in MDA formation,