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In vitro nephrotoxicity induced by propanil.

Gary O Rankin1, Christopher Racine, Adam Sweeney

  • 1Department of Pharmacology, Physiology and Toxicology, Joan C Edwards School of Medicine, Marshall University, One John Marshall Drive, Huntington, West Virginia 25755, USA. rankin@marshall.edu

Environmental Toxicology
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Propanil is a nephrotoxic herbicide, causing kidney cell damage in vitro. Its toxicity is not mainly from hydrolysis but may involve oxidative metabolites, with cytochrome P450 inhibition reducing damage.

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Area of Science:

  • Environmental toxicology
  • Renal cell biology
  • Herbicide metabolism

Background:

  • Propanil is a widely used herbicide in agriculture.
  • Known toxicities include methemoglobinemia, immunotoxicity, and nephrotoxicity.
  • The specific nephrotoxic potential and mechanisms of propanil remain underexplored.

Purpose of the Study:

  • To evaluate the in vitro nephrotoxic potential of propanil.
  • To investigate if propanil's nephrotoxicity stems from hydrolysis metabolites.
  • To explore the mechanistic pathways of propanil-induced kidney cell damage.

Main Methods:

  • Isolated renal cortical cells (IRCC) from male Fischer 344 rats were used.
  • Cells were exposed to propanil, 3,4-DCA, or propionic acid.
  • Cytotoxicity was measured via lactate dehydrogenase (LDH) release.
  • IRCC were pretreated with inhibitors of metabolic enzymes before propanil exposure.

Main Results:

  • Propanil induced significant cytotoxicity in IRCC at concentrations greater than 0.5 mM.
  • The major metabolite 3,4-dichloroaniline (3,4-DCA) also exhibited cytotoxicity.
  • Inhibition of cytochrome P450 enzymes with piperonyl butoxide reduced propanil-induced cytotoxicity.

Conclusions:

  • Propanil demonstrates in vitro nephrotoxicity in isolated renal cortical cells.
  • Propanil's kidney toxicity is not primarily mediated by hydrolysis products.
  • Oxidative metabolism, potentially involving cytochrome P450, may contribute to propanil's nephrotoxic effects.