Ciobică A, Hriţcu L, Artenie V, Pădurariu Manuela
School of Biology, Department of Molecular and Experimental Biology, "Alexandru Ioan Cuza" University Iaşi.
Rev Med Chir Soc Med Nat Iasi. 2009 Jul-Sep;113(3):832-7.
Reactive oxygen species (ROS) are produced within the body during oxygen metabolism and living organisms have developed several defense mechanisms to protect themselves from oxidative stress. Under normal conditions, ROS and antioxidant systems are in balance. Oxidative stress is caused by the imbalance between production of pro-oxidants and the antioxidant defenses. The defense mechanisms include antioxidant enzymes like superoxide dismutase (SOD) or glutathione peroxidase (GPX) and several no enzymatic free radical scavengers. It has been proposed that the progressive increase in ROS and consequent oxidative damage play the major role in neurodegenerative disorders. Learning and memory show an age-related decline and this age-associated impairment extends to spatial memory tasks. Furthermore, the neural circuits between the prefrontal cortex and striatum are also involved in spatial memory. In our previous studies, we have shown the facilitatory role of nicotine and cholinergic system in learning and memory processes. In the present study, we examined whether oxidative stress contributes to the memory deficits induced by muscarinic acetylcholine receptors (mAchRS) blocked by scopolamine. We also examined the effect of nicotine on oxidative stress, and also if nicotine could attenuated the learning and memory deficits induced by blocked of mAchRS. We observed that the levels of SOD and GPX decrease in rats mAchRS blockade by scopolamine (0.75 mg/kg body weight i.p.), and the level of malondialdehyde (MDA) increase in same rats, compared with saline-treated rats. Therefore, our results suggest that the oxidative stress contributes to the learning and memory deficits in rats.
活性氧（ROS）在机体氧气代谢过程中产生，生物体已发展出多种防御机制来保护自身免受氧化应激的影响。在正常情况下，ROS与抗氧化系统处于平衡状态。氧化应激是由促氧化剂生成与抗氧化防御之间的失衡所引起的。防御机制包括超氧化物歧化酶（SOD）或谷胱甘肽过氧化物酶（GPX）等抗氧化酶以及一些非酶自由基清除剂。有人提出，ROS的逐渐增加及随之而来的氧化损伤在神经退行性疾病中起主要作用。学习和记忆会随着年龄的增长而衰退，这种与年龄相关的损害也延伸到空间记忆任务。此外，前额叶皮质与纹状体之间的神经回路也参与空间记忆。在我们之前的研究中，我们已经证明了尼古丁和胆碱能系统在学习和记忆过程中的促进作用。在本研究中，我们研究了氧化应激是否导致东莨菪碱阻断毒蕈碱型乙酰胆碱受体（mAchRS）所诱导的记忆缺陷。我们还研究了尼古丁对氧化应激的影响，以及尼古丁是否能减轻mAchRS阻断所诱导的学习和记忆缺陷。我们观察到，与生理盐水处理的大鼠相比，东莨菪碱（0.75mg/kg体重腹腔注射）阻断大鼠mAchRS后，SOD和GPX水平降低，而丙二醛（MDA）水平升高。因此，我们的结果表明氧化应激导致大鼠的学习和记忆缺陷。
