HWA-448 reduces gentamicin toxicity in LLC-PK1 cells

J Pharmacol Exp Ther. 1995 Jul;274(1):29-33.

Abstract

An LLC-PK1 cell culture model was used to evaluate for a direct protective effect of the pentoxifylline analogue HWA-448 in gentamicin nephrotoxicity at the cellular level. Cells exposed to 2 mM gentamicin for 6 days displayed a significant decrease in specific activities of leucine aminopeptidase, NaK ATPase, and N-acetyl glucosaminidase, and an increase in total cellular phospholipids (P < .05). Concomitant exposure to 0.125 mM HWA-448, a dose that did not alter cellular enzymes or total phospholipids under physiologic conditions, prevented the alterations in marker enzymes and total phospholipids induced by gentamicin (P < .05). Gentamicin binding and uptake studies revealed 0.125 mM HWA-448 had no effect on LLC-PK1 cell plasma membrane binding or cellular gentamicin uptake. We conclude that HWA-448 ameliorates gentamicin-induced alterations in LLC-PK1 cell enzymes and phospholipids by a mechanism independent of plasma membrane binding or cellular uptake.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Drug Interactions
  • Gentamicins / antagonists & inhibitors
  • Gentamicins / toxicity*
  • LLC-PK1 Cells
  • Models, Biological
  • Pentoxifylline / analogs & derivatives*
  • Pentoxifylline / pharmacology
  • Sodium-Potassium-Exchanging ATPase / metabolism
  • Swine

Substances

  • Gentamicins
  • torbafylline
  • Sodium-Potassium-Exchanging ATPase
  • Pentoxifylline