Enache Mihaela, Van Waes Vincent, Vinner Elisabeth, Lhermitte Michel, Maccari Stefania, Darnaudéry Muriel
UPRES EA 4052, Equipe Stress Périnatal, Université de Lille 1, 59655 Villeneuve D'Ascq, France.
Brain Res. 2008 Jan 29;1191:55-62. doi: 10.1016/j.brainres.2007.11.031. Epub 2007 Nov 28.
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.
大鼠产前应激（PRS）与海马功能障碍以及与该脑区相关的几种行为和内分泌紊乱有关。最近，我们报道了PRS会改变青春期动物下丘脑-垂体-肾上腺（HPA）对乙醇刺激的反应。由于海马在青春期对乙醇的有害影响特别敏感，我们在本研究中调查了PRS和乙醇给药对28日龄雄性大鼠海马氧化状态的联合影响。腹腔注射乙醇（1.5 g/kg）30分钟后，检测了几种抗氧化酶（超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶）以及非酶抗氧化剂（还原型谷胱甘肽）的活性。还测量了硫代巴比妥酸反应性物质（TBARS）水平作为脂质过氧化的标志物。乙醇增强了对照大鼠中超氧化物歧化酶的活性，但在PRS大鼠中未增强。在基础水平上，PRS大鼠中的过氧化氢酶活性低于对照大鼠，表明在这种早期应激后对氧化损伤的潜在敏感性更高。然而，乙醇给药并未显著影响海马TBARS水平，表明急性乙醇暴露不会在青春期雄性大鼠中诱导氧化损伤。总之，我们的数据表明，PRS既影响海马的基础抗氧化状态，也影响急性乙醇暴露后的抗氧化反应。这些发现扩展了先前的研究成果，即PRS会导致海马功能障碍，并提出了重复暴露于乙醇后PRS大鼠海马氧化损伤潜在增加的问题。
