kidney papillary necrosis/glutathione

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Sulfur-containing amino acids that increase renal glutathione protect the kidney against papillary necrosis induced by 2-bromoethylamine.

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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

Investigation of regional glutathione levels in a model of chemically-induced renal papillary necrosis.

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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

Urinary metabolites of 2-bromoethanamine identified by stable isotope labelling: evidence for carbamoylation and glutathione conjugation.

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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

Biomarkers of collecting duct injury in Han-Wistar and Sprague-Dawley rats treated with N-phenylanthranilic Acid.

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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

Combination analgesic-induced kidney disease: the Australian experience.

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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

Changes in antioxidant enzyme activities and lipid peroxidation related to bromoethylamine-induced renal cytotoxicity.

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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,

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