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 Ca2+ levels because ethanol, at concentrations ranging from 0.1-0.5%, is able to decrease gp120-stimulated Ca2+ 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 Ca2+-activated, NO/cGMP-dependent mechanism.
Ethanol exposure inhibits the cytotoxic effect induced by gp120 in CHP100 human neuroblastoma cells
NAVARRA, Michele;
2001-01-01
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 Ca2+ levels because ethanol, at concentrations ranging from 0.1-0.5%, is able to decrease gp120-stimulated Ca2+ 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 Ca2+-activated, NO/cGMP-dependent mechanism.Pubblicazioni consigliate
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