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The effects of Cu and Se deficiency on cephaloridine nephrotoxicity in rats

Conference · · FASEB Journal (Federation of American Societies for Experimental Biology); (United States)
OSTI ID:5300808
; ;  [1]
  1. Univ. of Georgia, Athens (United States)

It has been proposed that nephrotoxicity of cephaloridine (CE), a betalactam antibiotic, is mediated via the production of oxygen radicals. Trace elements such as copper (Cu) and selenium (Se) are thought to play a role in protection against oxygen radical damage and Se deficiency has been shown to enhance CE nephrotoxicity. This study was conducted to compare the effects of Cu and Se nutrition on CE nephrotoxicity. Weanling, male, Sprague-Dawley rats were fed adequate, Cu deficient, Se deficient and Se and Cu deficient diets for 4 weeks and subsequently injected i.p. with CE or saline. CE treatment increase plasma urea, kidney weight, excretion of urinary enzymes and kidney pathology and decreased activity of kidney Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and glutathione peroxidase (GSH-Px). Se deficiency decreased kidney GSH-Px activity and increased CE nephrotoxicity with increased plasma urea, kidney weight, excretion of urinary enzymes and kidney pathology. Cu deficiency had no effect on CE nephrotoxicity but resulted in a small depression in kidney Cu,Zn-SOD activity. It is doubtful that the small change in kidney Cu,Zn-SOD activity would be sufficient to impair antioxidant status. In contrast the marked depression in GSH-Px activity during Se deficiency may have impaired antioxidant status, and contributed to an increase in CE nephrotoxicity.

OSTI ID:
5300808
Report Number(s):
CONF-9104107--
Journal Information:
FASEB Journal (Federation of American Societies for Experimental Biology); (United States), Journal Name: FASEB Journal (Federation of American Societies for Experimental Biology); (United States) Vol. 5:4; ISSN 0892-6638; ISSN FAJOE
Country of Publication:
United States
Language:
English