paperKB
coga / coga-kb
Help
Sign in

Chunk #4 — Introduction

Source
Mechanism of alcohol-induced oxidative stress and neuronal injury.
Embedded
yes

Text

in livers [36] and copper in kidneys/heart [37] has been reported in rats fed chronic alcohol diets, changes in metal ion concentrations in alcoholic brains are currently unknown. Here, we hypothesize that metabolism of EtOH by ADH and CYP2E1 generates ROS and NO in human neurons due to activation of NOX/XOX and inducible nitric oxide synthase (iNOS) by Ach. We observed that an induction of CYP2E1 activity parallels increased ROS and NO production in neurons after EtOH treatment. High levels of lipid peroxidation product, 4-hydroxynonenal, indicating cellular oxidative damage are accompanied by diminished expression of neuronal markers (neurofilaments) and enhanced neuronal death.