Valvassori Samira S, Fortunato Jucélia J, Gomes Karin M, Réus Gislaine Z, Martins Márcio R, Gavioli Elaine C, Schetinger Maria Rosa C, Dal-Pizzol Felipe, Quevedo João
Laboratório de Neurociencias, Programa de Pós-Graduacao em Ciencias da Saúde, Universidade do Extremo Sul Catrinense, 88806-000 Criciúma, SC, Brazil.
Neurotox Res. 2007 Jul;12(1):71-9. doi: 10.1007/BF03033902.
Malathion [S-(1,2-dicarbethoxy) ethyl-0,0-dimethyl-phosphorodithioate] is an organophosphorus compound that is widely used as pesticide especially in developing countries. This pesticide affects the central nervous system by inhibiting acetylcholinesterase, leading to an increase of acetylcholine in the synaptic cleft, and subsequent activation of cholinergic muscarinic and nicotinic receptors. In humans, intoxication with organophosphates causes a wide range of neurological symptoms, including memory deficits. The present study was aimed to investigate the effects of the acute (1 h prior the test) and subacute (once a day for 28 days) exposure to malathion at doses of 25, 50, 100 and 150 mg/kg in rats tested in the step-down inhibitory avoidance task, open-field habituation and elevated plus-maze tests. Interestingly, the acute and subacute treatment with malathion impaired aversive-memory in the step-down inhibitory avoidance task, but did not alter the animal performance in the elevated plus-maze and in the habituation to the open-field tests, and neither modified spontaneous locomotion. The activity of acetylcholinesterase enzyme was significantly reduced after subacute, but not acute, treatment with malathion (25, 100 and 150 mg/kg). Our results suggest that malathion impairs aversive-memory retention but not non-associative memory, without affecting anxiety-related behaviors. These findings support the view that the inhibition of acetylcholinesterase enzyme is not correlated with cognitive deficits observed in acute and subacute malathion-treated rats.
马拉硫磷[S-(1,2-二乙氧基羰基)乙基-0,0-二甲基硫代磷酸酯]是一种有机磷化合物,在发展中国家被广泛用作杀虫剂。这种杀虫剂通过抑制乙酰胆碱酯酶来影响中枢神经系统,导致突触间隙中乙酰胆碱增加,随后激活胆碱能毒蕈碱受体和烟碱受体。在人类中,有机磷中毒会导致广泛的神经症状,包括记忆缺陷。本研究旨在调查在大鼠的避暗抑制性回避任务、旷场习惯化和高架十字迷宫试验中,急性(试验前1小时)和亚急性(每天一次,持续28天)暴露于25、50、100和150mg/kg剂量的马拉硫磷的影响。有趣的是,马拉硫磷的急性和亚急性处理损害了避暗抑制性回避任务中的厌恶记忆,但没有改变动物在高架十字迷宫中的表现以及在旷场试验中的习惯化,也没有改变自发运动。亚急性(而非急性)处理马拉硫磷(25、100和150mg/kg)后,乙酰胆碱酯酶的活性显著降低。我们的结果表明,马拉硫磷损害厌恶记忆的保持,但不损害非联想记忆,且不影响焦虑相关行为。这些发现支持这样一种观点,即乙酰胆碱酯酶的抑制与急性和亚急性马拉硫磷处理的大鼠中观察到的认知缺陷无关。