Is thallium-induced nephrotoxicity in rats connected with riboflavin and/or GSH?--reconsideration of hypotheses on the mechanism of thallium toxicity.
Adult female Wistar rats (Han:Wist) were injected with 2 mg of Tl2SO4 per 100 g body weight. Parameters of nephrotoxicity were urinary volume and protein excretion as well as blood urea nitrogen concentration. Thallium concentrations were determined in renal cortex and medulla. There was no effect of different schedules of vitamin B2 (riboflavin) treatment on thallium nephrotoxicity. Glutathione (GSH) concentration was not decreased by thallium in renal cortex or in medulla. The increase of GSH concentration in renal tissue by N-acetylcysteine pretreatment did not influence thallium nephrotoxicity. Buthionine sulphoximine diminished thallium nephrotoxicity by a significant decrease of thallium concentration in renal medulla, which was caused by enhanced urinary excretion of thallium. From our investigations we conclude that there is no relation between thallium-induced nephrotoxicity and riboflavin and/or GSH.
Appenroth
D
D
Institute of Pharmacology and Toxicology, Friedrich Schiller University, Jena, Germany.
Winnefeld
K
K
D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D001806:Blood Urea Nitrogen; D019328:Buthionine Sulfoximine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D005260:Female; D005978:Glutathione / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects*; D011507:Proteinuria / Q000209:etiology; D051381:Rats; D017208:Rats, Wistar; D012256:Riboflavin / Q000378:metabolism*; D013793:Thallium / Q000493:pharmacokinetics / Q000633:toxicity*