A neurotoxic alcohol exposure paradigm does not induce hepatic encephalopathy.

Autor: Hashimoto JG; Research & Development Service, VA Portland Health Care System, Portland, OR, USA; Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR, USA., Wiren KM; Research & Development Service, VA Portland Health Care System, Portland, OR, USA; Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR, USA., Wilhelm CJ; Research & Development Service, VA Portland Health Care System, Portland, OR, USA; Department of Psychiatry, Oregon Health & Science University, Portland, OR, USA. Electronic address: wilhelmc@ohsu.edu.
Jazyk: angličtina
Zdroj: Neurotoxicology and teratology [Neurotoxicol Teratol] 2016 Jul-Aug; Vol. 56, pp. 35-40. Date of Electronic Publication: 2016 Jun 04.
DOI: 10.1016/j.ntt.2016.06.001
Abstrakt: Alcohol abuse is associated with neurological dysfunction, brain morphological deficits and frank neurotoxicity. Although these disruptions may be a secondary effect due to hepatic encephalopathy, no clear evidence of causality is available. This study examined whether a 72h period of alcohol intoxication known to induce physical dependence, followed by a single withdrawal, was sufficient to induce signs of hepatic encephalopathy in male and female mice. Animals were continuously intoxicated via alcohol vapor inhalation, a procedure previously shown to induce significant neurotoxicity in female mice. At peak synchronized withdrawal (8h following the end of alcohol exposure), blood samples were taken and levels of several liver-regulated markers and brain swelling were characterized. Glutathione levels were also determined in the medial frontal cortex (mFC) and hippocampus. Results revealed elevated levels of cholesterol, albumin, alkaline phosphatase (ALP), alanine aminotransferase (ALT) and decreased levels of blood urea nitrogen and total bilirubin in alcohol-exposed male and female groups compared to controls. Brain water weight was not affected by alcohol exposure, though males tended to have slightly more water weight overall. Alcohol exposure led to reductions in tissue levels of glutathione in both the hippocampus and mFC which may indicate increased oxidative stress. Combined, these results suggest that hepatic encephalopathy does not appear to play a significant role in the neurotoxicity observed following alcohol exposure in this model.
(Published by Elsevier Inc.)
Databáze: MEDLINE
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