Nephrotoxicity pp 457-461 | Cite as

The Role of Oxidative Stress in Cephaloridine Nephrotoxicity

  • Robin S. Goldstein
  • Randall S. Sozio
  • Joan B. Tarloff
  • Jerry B. Hook

Abstract

The cephalosporin antibiotic, cephaloridine (CPH), is nephrotoxic when administered in large dosages to humans and laboratory animals (1,2) . In vivo, CPH nephrotoxicity is characterized histologically by acute proximal tubular necrosis and functionally by glycosuria, enzymuria, proteinuria and an impaired ability of renal cortical slices to accumulate organic ions (1-4). Previous studies have indicated that the nephrotoxicity of CPH is intimately related to its renal cortical accumulation and intracellular concentration (5). CPH is actively transported into the proximal tubule cell by an organic anion transport system (5,6). However, unlike many organic anions and cephalosporins, CPH undergoes only limited movement across the lumenal membrane into the tubular fluid. Consequently, high intracellular concentrations of CPH are attained in the proximal tubule which are critical to the development of nephrotoxicity (5).

Keywords

Proximal Tubular Cell High Intracellular Concentration Intracellular Thiol Renal Cortical Slice Generate Oxygen Free Radical 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1989

Authors and Affiliations

  • Robin S. Goldstein
    • 1
  • Randall S. Sozio
    • 1
  • Joan B. Tarloff
    • 1
  • Jerry B. Hook
    • 1
  1. 1.Smith Kline & French LaboratoriesDepartment of Investigative ToxicologyKing of PrussiaUSA

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