dc.creatorBoveris, Alberto
dc.creatorLlesuy, Susana
dc.creatorAzzalis, Ligia A.
dc.creatorGiavarotti, Leandro
dc.creatorSimon, Karin A.
dc.creatorJunqueira, Virginia
dc.creatorPorta, Eduardo A.
dc.creatorVidela Cabrera, Luis
dc.creatorLissi Gervaso, Eduardo A.
dc.date.accessioned2019-01-29T17:15:45Z
dc.date.available2019-01-29T17:15:45Z
dc.date.created2019-01-29T17:15:45Z
dc.date.issued1997
dc.identifierToxicology Letters, Volumen 93, Issue 1, 2018, Pages 23-28
dc.identifier03784274
dc.identifier10.1016/S0378-4274(97)00066-0
dc.identifierhttp://repositorio.uchile.cl/handle/2250/163320
dc.description.abstractThe influence of acute ethanol administration on the oxidative stress status of rat brain and liver was assessed by in situ spontaneous organ chemiluminescence (CL). Brain and liver CL was significantly increased after acute ethanol administration to fed rats, a response that is time-dependent and evidenced at doses higher than 1 g/kg. Ethanol-induced CL development is faster in liver compared with brain probably due to the greater ethanol metabolic capacity of the liver, whereas the net enhancement in brain light emission at 3 h after ethanol treatment is higher than that of the liver, which could reflect the greater susceptibility of brain to oxidative stress. The effect of ethanol on brain and liver CL seems to be mediated by acetaldehyde, due to its abolishment by the alcohol dehydrogenase inhibitor 4-methylpyrazole and exacerbation by the aldehyde dehydrogenase inhibitor disulfiram. In brain, these findings were observed in the absence of changes in the activity of superoxide dism
dc.languageen
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceToxicology Letters
dc.subjectAntioxidants
dc.subjectBrain
dc.subjectChemiluminescence
dc.subjectEthanol
dc.subjectLiver
dc.subjectOxidative stress
dc.titleIn situ rat brain and liver spontaneous chemiluminescence after acute ethanol intake
dc.typeArtículos de revistas


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