Acute toxicity of cephaloridine, an antibiotic derived from cephalosporin C

Possible role of cysteine-S-conjugate β-lyase in species differences in cisplatin nephrotoxicity

“…Alternatively, further studies are needed to quantitatively grasp the reactive (toxic) metabolites of cisplatin in the renal cortex. Generally, the rabbit is well known to possess high susceptibility to nephrotoxic agents including antibiotics compared with rats (Atkinson et al 1966); therefore, this species is frequently used for early screening of novel pharmaceutical candidates. Our findings that cisplatin nephrotoxicity was stronger in rats than in rabbits were extremely interesting.…”

Changes in lipid peroxidation and activities of xanthine oxidase, superoxide dismutase and catalase in kidneys of cephaloridine-administered rats.

“…As regards to the CER ne phrotoxicity in experimental animals, the fol lowing findings have been reported: suppres sion of the renal organic anion transport sys tem, reduced glomerular filtration rates, glu cosuria, proteinuria and others, which were observed in physiological studies (3,4); inhi bition of gluconeogenesis, inhibition of respi ration in mitochondria and decrement in re duced glutathione content in the renal cor tex, as observed by biological studies (5-7); nuclear pyknosis, cytoplasmic disintegration, hydropic changes and necrosis in the proximal tubular cells, and patchy loss of the brush border membranes in the proximal tubules, as determined by histopathological studies (1,2). Several biochemical mechanisms respon sible for the CER-nephrotoxicity have been proposed (5,(8)(9)(10)(11)(12), while its precise toxic mechanisms remain to be investigated.…”

“…(CER), one of the cepha losporins, is known to produce renal injury in humans and laboratory animals, and its main toxic effect is considered to be on the proxi mal tubules (1,2). As regards to the CER ne phrotoxicity in experimental animals, the fol lowing findings have been reported: suppres sion of the renal organic anion transport sys tem, reduced glomerular filtration rates, glu cosuria, proteinuria and others, which were observed in physiological studies (3,4); inhi bition of gluconeogenesis, inhibition of respi ration in mitochondria and decrement in re duced glutathione content in the renal cor tex, as observed by biological studies (5-7); nuclear pyknosis, cytoplasmic disintegration, hydropic changes and necrosis in the proximal tubular cells, and patchy loss of the brush border membranes in the proximal tubules, as determined by histopathological studies (1,2).…”

Effects of KW-3902, a Novel Adenosine A1-Receptor Antagonist, on Cephaloridine-Induced Acute Renal Failure in Rats

“…However, use of an excessive dosage of CER produces renal injury in humans as well as in laboratory animals (2)(3)(4). The main toxic effect of CER has been ascribed to the action of this drug on the proximal tubule (5,6). Suppression of the renal organic anion transport system, reduced glomerular filtration rates, glucosuria, proteinuria, and other effects were ob served following the administration of CER (7)(8)(9).…”

“…Suppression of the renal organic anion transport system, reduced glomerular filtration rates, glucosuria, proteinuria, and other effects were ob served following the administration of CER (7)(8)(9). Histopathological studies (5,6,10) demonstrated nuclear pyknosis, cytoplasmic disintegration, hydropic changes and necrosis in the proximal tubular cells and patchy loss of the brushborder membranes in the proximal tubule. Several mechanisms for the CER-induced nephrotoxicity have been proposed.…”