Rehabilitating role of glutathione ester on cisplatin induced nephrotoxicity

Ren Fail. 1999 Mar;21(2):209-17. doi: 10.3109/08860229909066985.

Abstract

Cisplatin caused differential toxic effects on blood glucose and plasma urea, uric acid and creatinine levels. Cisplatin also showed an inhibitory effect on kidney marker enzymes like alkaline phosphatase, acid phosphatase, aspartate aminotransferase and alanine aminotransferase. However, administration of glutathione ester modulates the toxic side effect of cisplatin observed in kidney enzymes, and in blood parameters. It seems that glutathione ester plays an important role in protecting against the cisplatin induced nephrotoxicity by inhibiting the accumulation of platinum in kidneys.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / toxicity*
  • Biomarkers
  • Cisplatin / toxicity*
  • Creatinine / blood
  • Disease Models, Animal
  • Esters / pharmacology
  • Glutathione / pharmacology*
  • Kidney / drug effects*
  • Kidney / enzymology
  • Kidney Diseases / blood
  • Kidney Diseases / chemically induced
  • Kidney Diseases / prevention & control*
  • Male
  • Phosphoric Monoester Hydrolases / metabolism
  • Rats
  • Rats, Wistar
  • Transferases / metabolism
  • Urea / blood
  • Uric Acid / blood

Substances

  • Antineoplastic Agents
  • Biomarkers
  • Esters
  • Uric Acid
  • Urea
  • Creatinine
  • Transferases
  • Phosphoric Monoester Hydrolases
  • Glutathione
  • Cisplatin