title: Impact of an acute exposure to ethanol on the oxidative stress status in the hippocampus of prenatal restraint stress adolescent male rats.
abstract: Prenatal restraint stress (PRS) in rats is associated with hippocampal dysfunctions and several behavioural and endocrine disorders related to this brain area. Recently, we have reported that the PRS modifies the hypothalamic-pituitary-adrenal (HPA) response to an ethanol challenge in adolescent animals. Since hippocampus is particularly sensitive to the deleterious effects of ethanol during adolescence, we investigated in this study the combined effects of PRS and ethanol administration on the oxidative status in the hippocampus of 28-day-old male rats. Thirty minutes after an intraperitoneal (i.p.) injection of ethanol (1.5 g/kg), the activities of several antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) but also non-enzymatic antioxidant (reduced glutathione) were assayed. Thiobarbituric acid reactive substances (TBARS) levels were also measured as a marker of lipid peroxidation. Ethanol enhanced superoxide dismutase activity in control rats but not in PRS rats. At basal level, catalase activity was lower in PRS rats than in control rats, indicating a potentially higher sensitivity to oxidative damages after this early stress. However, the hippocampal TBARS levels were not significantly affected by the ethanol administration, showing that an acute ethanol exposure does not induce oxidative damage in adolescent male rats. In conclusion, our data suggest that PRS affects both basal antioxidant status in the hippocampus and antioxidant response after an acute ethanol exposure. These findings extend previous works showing that PRS leads to hippocampal dysfunctions and raise the question of the potential increase of the hippocampal oxidative damage in PRS rats after repeated exposure to ethanol.
authors: UPRES EA 4052, Equipe Stress Périnatal, Université de Lille 1, 59655 Villeneuve D'Ascq, France.
authors: Mihaela
authors: M
authors: Enache
authors: Vincent
authors: V
authors: Van Waes
authors: Elisabeth
authors: E
authors: Vinner
authors: Michel
authors: M
authors: Lhermitte
authors: Stefania
authors: S
authors: Maccari
authors: Muriel
authors: M
authors: Darnaudéry
mesh_terms: D000367:Age Factors; D000435:Alcoholic Intoxication / Q000150:complications / Q000201:enzymology*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002374:Catalase / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D000431:Ethanol / Q000494:pharmacology; D005260:Female; D005978:Glutathione / Q000187:drug effects / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000187:drug effects / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology* / Q000254:growth & development; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D010088:Oxidoreductases / Q000187:drug effects / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000201:enzymology*; D051381:Rats; D012149:Restraint, Physical; D013315:Stress, Psychological / Q000150:complications / Q000201:enzymology*; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017392:Thiobarbituric Acid Reactive Substances; D000431:Ethanol; D010088:Oxidoreductases; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione