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ABSTRACT: High-altitude hypoxia impedes cognitive performance. It is not well known whether the prophylactic use of acetazolamide for altitude sickness can influence cognitive performance at high altitude. When ascending to high altitude locations, one may face medical risks, including cognitive impairment, which may significantly hinder climbing abilities or exploratory behavior. Effective prophylactic drugs have rarely been reported. Because acetazolamide is commonly used to treat acute mountain sickness (AMS), we assessed the potential effects of acetazolamide on cognitive performance during high-altitude exposure. Twenty-one volunteers aged 22-26 years were randomized to receive a 4-day treatment of acetazolamide (125 mg Bid, n=11) or placebo (n=10) before and after air travel from Xianyang (402 m) to Lhasa (3561 m). Neuropsychological performance was assessed using the digit symbol substitution test (DSST), paced auditory serial addition test (PASAT), operation span task, and free recall test at 6, 30, and 54 hours after arrival at Lhasa. The Lake Louise Score (LLS) was used to diagnose AMS. At high altitude, acetazolamide impaired rather than improved neuropsychological measures of concentration, cognitive processing speed, reaction time, short-term memory, and working memory, which were assessed by DSST, PASAT, and operation span task at 6 and 30 hours after arrival (p<0.05). However, the prophylactic use of acetazolamide was found to reduce the incidence of AMS compared to the placebo (p<0.05). In conclusion, acetazolamide impairs neuropsychological function, at least in part, shortly after the ascent to high altitude.
Neurotoxicology and Teratology 12/2012; · 2.98 Impact Factor
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Jinfei Jing,
Gang Zheng,
Mingchao Liu,
Xuefeng Shen,
Fang Zhao, Jiye Wang,
Jianbin Zhang,
Guanpeng Huang,
Peng Dai,
Yinglei Chen,
Jingyuan Chen,
Wenjing Luo
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ABSTRACT: Many epidemiological studies and in vitro experiments have found that chronic arsenic exposure may influence memory formation. The goal of this study was to create an animal model of memory impairment induced by chronic arsenite exposure and to study the underlying mechanisms. Sixty male Sprague-Dawley (SD) male rats were randomly divided into a control group, a low-dose sodium arsenite exposure group and a high-dose sodium arsenite exposure group. Sodium arsenite was administered by adding it to drinking water for 3 months. Then, the spatial memory of the rats was examined with Morris water maze and Y maze. The concentration of arsenic in the blood and the brain was determined by an atomic fluorescence absorption spectrometer. The ultra-structure of hippocampal neurons was observed by an electron microscope. Timm staining was used for observing mossy fibers. We found that the concentration of arsenic in the blood and the brain increased in a dose-response manner (P<0.05). The performance of rats in the arsenite exposed group (15mg/kg) was significantly impaired in the Morris water maze and Y maze tasks than those in the control group (P<0.05). Sodium arsenite exposure resulted in abnormal structural changes in the myelin sheaths of nerve fibers and decreases in the terminals of mossy fibers. Together, chronic sodium arsenite exposure through drinking water results in detrimental changes in the neuronal synapses, which may contribute to the arsenite-induced impairment of spatial memory.
NeuroToxicology 07/2012; 33(5):1230-8. · 3.10 Impact Factor
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ABSTRACT: To study the toxicity and its mechanisms of 1-methyl-4-phenylpyridinium ion (MPP+) on pheochromocytoma PC12 cells.
PC12 cells were cultured in vitro, and poisoned by 100, 300, 500 micromol/L MPP+. Western blot was performed to determine the level of phosphorylated c-Jun-N-terminal kinase/stress activated protein kinases (JNK/SAPK). The cells were pretreated with SP600125, an inhibitor of JNK pathway, and then the number of apoptotic cells were counted by using TUNEL stain, observing its influence on cell apoptosis seduced by MPP+.
MPP+ poisoning can cause the increase of phosphorylation level of JNK1/2 cells. The usage of JNK pathway inhibitor SP600125 can inhibit the PC12 cell apoptosis seduced by MPP+.
Activation of JNK pathway may be the important molecular mechanism of PC12 cell apoptosis seduced by MPP+ and of producing dopaminergic neurotoxicity.
Wei sheng yan jiu = Journal of hygiene research 01/2011; 40(1):109-11.
