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Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> is centrally metabolized into acetaldehyde, which has been shown to be responsible for some of the neurophysiological and cellular effects of Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>. Although some of the consequences of chronic Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> administration on cell oxidative status have been described, the mechanisms by which acute Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> administration affects the brain's cellular oxidative status and the role of acetaldehyde remain to be elucidated in detail.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Swiss <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\u2010I mice were pretreated with the acetaldehyde\u2010sequestering agent <jats:sc>d<\/jats:sc>\u2010penicillamine (<jats:styled-content style=\"fixed-case\">DP<\/jats:styled-content>; 75\u00a0mg\/kg, i.p.) or the antioxidant lipoic acid (<jats:styled-content style=\"fixed-case\">LA<\/jats:styled-content>; 50\u00a0mg\/kg, i.p.) 30\u00a0minutes before Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> (2.5\u00a0g\/kg, i.p.) administration. Animals were sacrificed 30\u00a0minutes after Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> injection. Glutathione peroxidase (<jats:styled-content style=\"fixed-case\">GP<\/jats:styled-content>x) <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> levels; <jats:styled-content style=\"fixed-case\">GP<\/jats:styled-content>x and glutathione reductase (<jats:styled-content style=\"fixed-case\">GR<\/jats:styled-content>) enzymatic activities; reduced glutathione (<jats:styled-content style=\"fixed-case\">GSH<\/jats:styled-content>), glutathione disulfide (<jats:styled-content style=\"fixed-case\">GSSG<\/jats:styled-content>), glutamate, g\u2010L\u2010glutamyl\u2010L\u2010cysteine (Glut\u2010Cys), and malondialdehyde (<jats:styled-content style=\"fixed-case\">MDA<\/jats:styled-content>) concentrations; and protein carbonyl group (<jats:styled-content style=\"fixed-case\">CG<\/jats:styled-content>) content were determined in whole\u2010brain samples.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Acute Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> administration enhanced <jats:styled-content style=\"fixed-case\">GP<\/jats:styled-content>x activity and the <jats:styled-content style=\"fixed-case\">GSH<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">GSSG<\/jats:styled-content> ratio, while it decreased <jats:styled-content style=\"fixed-case\">GR<\/jats:styled-content> activity and <jats:styled-content style=\"fixed-case\">GSSG<\/jats:styled-content> concentration. Pretreatment with <jats:styled-content style=\"fixed-case\">DP<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">LA<\/jats:styled-content> only prevented <jats:styled-content style=\"fixed-case\">GP<\/jats:styled-content>x activity changes induced by Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Altogether, these results show the capacity of a single dose of Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> to unbalance cellular oxidative homeostasis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.14133","type":"journal-article","created":{"date-parts":[[2019,6,18]],"date-time":"2019-06-18T18:48:02Z","timestamp":1560883682000},"page":"1672-1681","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Effects of Acute Ethanol Administration on Brain Oxidative Status: The Role of 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