<abstract xml:lang="en" xmlns="http://www.w3.org/1999/xhtml">This study compared the effects of toxicity of ethanol and its first metabolite acetaldehyde in rat astrocytes through cell viability and cell proliferation. The cells were treated with different concentrations of ethanol in the presence or absence of a catalase inhibitor 2-amino-1,2,4 triazole (AMT) or with different concentrations of acetaldehyde. Cell viability was assessed using the trypan blue test. Cell proliferation was assessed after 24 hours and after seven days of exposure to either ethanol or acetaldehyde.We showed that both ethanol and acetaldehyde decreased cell viability in a dose-dependent manner. In proliferation studies, after seven days of exposure to either ethanol or acetaldehyde, we observed a significant dose-dependent decrease in cell number. The protein content study showed biphasic dose-response curves, after 24 hours and seven days of exposure to either ethanol or acetaldehyde. Co-incubation in the presence of AMT significantly reduced the inhibitory effect of ethanol on cell proliferation.We concluded that long-term exposure of astrocytes to ethanol is more toxic than acute exposure. Acetaldehyde is a much more potent toxin than ethanol, and at least a part of ethanol toxicity is due to ethanol's first metabolite acetaldehyde.</abstract>

This study compared the effects of toxicity of ethanol and its first metabolite acetaldehyde in rat astrocytes through cell viability and cell proliferation. The cells were treated with different concentrations of ethanol in the presence or absence of a catalase inhibitor 2-amino-1,2,4 triazole (AMT) or with different concentrations of acetaldehyde. Cell viability was assessed using the trypan blue test. Cell proliferation was assessed after 24 hours and after seven days of exposure to either ethanol or acetaldehyde.We showed that both ethanol and acetaldehyde decreased cell viability in a dose-dependent manner. In proliferation studies, after seven days of exposure to either ethanol or acetaldehyde, we observed a significant dose-dependent decrease in cell number. The protein content study showed biphasic dose-response curves, after 24 hours and seven days of exposure to either ethanol or acetaldehyde. Co-incubation in the presence of AMT significantly reduced the inhibitory effect of ethanol on cell proliferation.We concluded that long-term exposure of astrocytes to ethanol is more toxic than acute exposure. Acetaldehyde is a much more potent toxin than ethanol, and at least a part of ethanol toxicity is due to ethanol's first metabolite acetaldehyde.

Comparison of Ethanol and Acetaldehyde Toxicity in Rat Astrocytes in Primary Culture

Poison Control Centre, University Medical Centre, Ljubljana

Faculty of Medicine, University of Ljubljana, Ljubljana

Faculty of Medicine, University of Maribor, Maribor, Slovenia

Archives of Industrial Hygiene and Toxicology

This study compared the effects of toxicity of ethanol and its first metabolite acetaldehyde in rat astrocytes through cell viability and cell proliferation....

Comparison of Ethanol and Acetaldehyde Toxicity in Rat Astrocytes in Primary Culture

Pubblicato online: 29 set 2009

Pagine: 297 - 305

DOI: https://doi.org/10.2478/10004-1254-60-2009-1927

Parole chiave
AMT, proliferacija, tripansko modrilo, viabilnost

This content is open access.

Comparison of Ethanol and Acetaldehyde Toxicity in Rat Astrocytes in Primary Culture

Pubblicato online: 29 set 2009

Pagine: 297 - 305

DOI: https://doi.org/10.2478/10004-1254-60-2009-1927

Parole chiaveAMT, proliferacija, tripansko modrilo, viabilnost

This content is open access.

Parole chiave
AMT, proliferacija, tripansko modrilo, viabilnost