Effects of Acute Ethanol Administration on Brain Oxidative Status: The Role of Acetaldehyde
Impacto
Scholar |
Otros documentos de la autoría: Baliño, Pablo; Romero Cano, Ricard; Sanchez-Andres, Juan V.; Valls, Victoria; González Aragón, Carlos Manuel; Muriach, Maria
Metadatos
Mostrar el registro completo del ítemcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/36080
comunitat-uji-handle3:10234/36082
comunitat-uji-handle4:
INVESTIGACIONEste recurso está restringido
https://doi.org/10.1111/acer.14133 |
Metadatos
Título
Effects of Acute Ethanol Administration on Brain Oxidative Status: The Role of AcetaldehydeAutoría
Fecha de publicación
2019-08Editor
WileyISSN
0145-6008; 1530-0277Cita bibliográfica
BALIÑO, Pablo, et al. Effects of acute ethanol administration on brain oxidative status: the role of acetaldehyde. Alcoholism: Clinical and Experimental Research, 2019, vol. 43, no 8, p.1672-1681Tipo de documento
info:eu-repo/semantics/articleVersión de la editorial
https://onlinelibrary.wiley.com/doi/full/10.1111/acer.14133Versión
info:eu-repo/semantics/publishedVersionPalabras clave / Materias
Resumen
Background:
Ethanol (EtOH), one of the most widely consumed substances of abuse, can induce brain damage and neurodegeneration. EtOH is centrally metabolized into acetaldehyde, which has been shown to be responsible ... [+]
Background:
Ethanol (EtOH), one of the most widely consumed substances of abuse, can induce brain damage and neurodegeneration. EtOH is centrally metabolized into acetaldehyde, which has been shown to be responsible for some of the neurophysiological and cellular effects of EtOH. Although some of the consequences of chronic EtOH administration on cell oxidative status have been described, the mechanisms by which acute EtOH administration affects the brain's cellular oxidative status and the role of acetaldehyde remain to be elucidated in detail.
Methods:
Swiss CD‐I mice were pretreated with the acetaldehyde‐sequestering agent d‐penicillamine (DP; 75 mg/kg, i.p.) or the antioxidant lipoic acid (LA; 50 mg/kg, i.p.) 30 minutes before EtOH (2.5 g/kg, i.p.) administration. Animals were sacrificed 30 minutes after EtOH injection. Glutathione peroxidase (GPx) mRNA levels; GPx and glutathione reductase (GR) enzymatic activities; reduced glutathione (GSH), glutathione disulfide (GSSG), glutamate, g‐L‐glutamyl‐L‐cysteine (Glut‐Cys), and malondialdehyde (MDA) concentrations; and protein carbonyl group (CG) content were determined in whole‐brain samples.
Results:
Acute EtOH administration enhanced GPx activity and the GSH/GSSG ratio, while it decreased GR activity and GSSG concentration. Pretreatment with DP or LA only prevented GPx activity changes induced by EtOH.
Conclusions:
Altogether, these results show the capacity of a single dose of EtOH to unbalance cellular oxidative homeostasis. [-]
Publicado en
Alcoholism: Clinical and Experimental Research, 2019, vol. 43, no 8Proyecto de investigación
Generalitat Valenciana; PROMETEO/2016/094; GV/2017/096; Universitat Jaume I, Spain: UJI-A2016-03Derechos de acceso
Copyright © John Wiley & Sons, Inc.
http://rightsstatements.org/vocab/InC/1.0/
info:eu-repo/semantics/restrictedAccess
http://rightsstatements.org/vocab/InC/1.0/
info:eu-repo/semantics/restrictedAccess
Aparece en las colecciones
- PSB_Articles [1291]
- MED_Articles [632]