Ethanol exposure inhibits the cytotoxic effect induced by gp120 in CHP100 human neuroblastoma cells

J Neurosci Res. 2001 Aug 15;65(4):354-61. doi: 10.1002/jnr.1161.

Abstract

The aim of present study was to investigate the acute effects of ethanol on cytotoxicity induced by HIV-1 coat protein gp120 in CHP100 human neuroblastoma cell line. We demonstrate that ethanol, within a range of clinically relevant concentrations (15-90 mM) prevents cell death elicited by gp120 (10 pM) in a dose dependent manner. This protective action seems to be mediated by a reduction of free intracellular Ca(2+) levels because ethanol, at concentrations ranging from 0.1-0.5%, is able to decrease gp120-stimulated Ca(2+) uptake up to 24%. Furthermore, our data show an involvement of NO/cGMP messenger system pathway, because ethanol is also able to reduce gp120-stimulated NO release (up to 45%) and cyclic GMP accumulation (up to 73%). These findings suggest that the protective effect of ethanol against gp120-induced cytotoxicity in CHP100 cells underlies a Ca(2+)-activated, NO/cGMP-dependent mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calcium / metabolism
  • Cell Death / drug effects
  • Central Nervous System Depressants / pharmacology*
  • Cyclic GMP / metabolism
  • Dose-Response Relationship, Drug
  • Ethanol / pharmacology*
  • Excitatory Amino Acid Agonists / pharmacology
  • HIV Envelope Protein gp120 / toxicity*
  • Humans
  • N-Methylaspartate / pharmacology
  • Neuroblastoma*
  • Neurons / cytology
  • Neurons / drug effects*
  • Neurons / metabolism
  • Nitric Oxide / metabolism
  • Tumor Cells, Cultured

Substances

  • Central Nervous System Depressants
  • Excitatory Amino Acid Agonists
  • HIV Envelope Protein gp120
  • Nitric Oxide
  • Ethanol
  • N-Methylaspartate
  • Cyclic GMP
  • Calcium