The effect of Tl2SO4 (Tl, 20 mg kg-1 body wt.) on renal function was investigated in 10- and 20-day-old rats. Nephrotoxic effects were evaluated by the determination of glomerular filtration rate, urinary volume, electrolyte and protein excretion, as well as by morphological investigations. In contrast to adult rats there were no morphological destructions in 10- and 20-day-old rats. Changes in renal function seemed to be less expressed in 10- and 20-day-old than in adult rats. The smaller nephrotoxicity in 10-day-old rats may be caused by lower Tl concentration in renal tissue, whereas in 20-day-old rats decreased nephrotoxicity cannot be explained in this way. The activity of Na+/K(+)-ATPase in rat renal tissues was found to be involved in the mechanisms of Tl enrichment in renal tissue, being an indirect determinant of Tl nephrotoxicity.

Animals↗

PubMedDate not supplied

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.

Acetylcysteine↗

PubMedDate not supplied

Beneficial effect of acetylcysteine on cisplatin nephrotoxicity in rats.

The influence of acetylcysteine (ac-cys) on cisplatin (CP) nephrotoxicity was investigated in female Wistar rats. Administration of 0.6 mg CP 100 g-1 body wt. was followed by oliguria and proteinuria, as well as a significant increase of blood urea nitrogen concentration. The i.p. administration of 0.6 mg CP 100 g-1 body wt. concomitantly with 100 mg ac-cys 100 g-1 body wt. s.c. completely abolished the nephrotoxic effects of CP. However, following this, the Pt concentration in kidney was decreased significantly by ac-cys treatment. This was caused by the enhanced urinary excretion of Pt. The same effect on CP nephrotoxicity appeared when CP and ac-cys were dissolved together in solution prior to injection. It could be shown that in this solution a ligand exchange reaction of CP by ac-cys started immediately, resulting in increased renal excretion and decreased Pt concentration in kidney. From our results we concluded that the protective effect of ac-cys on CP nephrotoxicity is based on the formation of a complex unsuitable for tubular reabsorption.

Acetylcysteine↗