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作 者:李祥[1] 汤艳[1] 吴雨岭[2] 于雪岚[3] 刘扬[3]
机构地区:[1]泸州医学院公共卫生系环卫与劳卫教研室,四川泸州646000 [2]泸州医学院组胚教研室,646000 [3]泸州医学院预防医学专业2007级,646000
出 处:《中国职业医学》2011年第6期463-466,共4页China Occupational Medicine
基 金:四川省教育厅基金项目(08zb086)
摘 要:目的观察十溴联苯醚(BDE-209)对成年大鼠学习记忆及海马神经元氧化应激和凋亡的影响。方法将96只SD雄性大鼠随机分为溶剂对照组、BDE-209低(250 mg/kg)、中(500 mg/kg)、高(1 000 mg/kg)剂量组,每天灌胃1次,持续30 d。用Morris水迷宫检测学习记忆功能,化学比色法测定大鼠海马组织总抗氧化能力(T-AOC)、谷胱甘肽转移酶(GST)、超氧化物歧化酶(SOD)、丙二醛(MDA)的水平,考马斯亮蓝法测定蛋白水平,末端标记(TUNEL)法检测海马CA1区神经元凋亡。结果与对照组比较,BDE-209染毒组大鼠的平均逃避潜伏期明显增加、空间搜索有效策略百分比和穿越平台的次数明显减少(P<0.05);且随染毒剂量的增加,BDE-209各组的平均逃避潜伏期明显增加、空间搜索有效策略百分比和穿越平台的次数明显减少(P<0.05)。BDE-209染毒组海马T-AOC、GST和SOD的活力明显低于对照组,MDA水平明显高于对照组(P<0.05);并随染毒剂量的增加各染毒组T-AOC、GST和SOD的活力明显降低,MDA水平明显增加(P<0.05)。TUNEL法检测结果显示BDE-209染毒组较对照组染色深,凋亡细胞数明显增加(P<0.05);BDE-209染毒组随染毒剂量的增加染色加深,凋亡细胞增加(P<0.05) BDE-209致成年大鼠学习记忆能力下降可能与海马神经元细胞氧化损伤和凋亡有关。Objective To observe the effects of brominated diphenyl ethers-209 (BDE-209) exposure on spatial learning memory abilities, oxidative damage, and apoptosis in hippocampal neurons of adult rats. Methods 96 healthy male SD rats were randomly divided into 4 groups, including a solvent control group and 3 BDE-209-treated groups (250, 500, 1000 mg/kg). The exposure groups were treated by garage once a day for 30 days. The capability of learning memory of rats were measured by Morris water maze test. The levels of total oxidizing ability (T-AOC), glutathioue transferase (GST), super oxide dismutase (SOD) and malonaldehyde (MDA) in hippocampal neurons were detected by chemical colorimetry. The apoptosis in hippocampal neurons were detected by TUNEL. Results Compared with those of the control, the escape latency was increased, the resourceful percentage and numbers of animals crossing the exact location of the original platform were decreased (P 〈 0. 05). As the exposure dosage increased, the latencies were increased and the resourceful percentage and numbers of animals crossing the exact location of the original platform were decreased ( P 〈 0.05 ). The activities of T-AOC, GST and SOD in hippo- eampal neurons were lower, while the content of MDA was higher than that of the control (P 〈 0. 05 ). Along with the dosage increased, the activities of T-AOC, GST and SOD were decreased, the content of MDA was increased ( P 〈 0. 05 ). The number of apoptosis in hippocampal neurons was higher than that of the control, and the number of apoptosis was increased with the dosage ( P 〈 0. 05 ). Conclusion The degression of learning memory abilities of adult rats induced by BDE-209 exposure may be related with the oxidative damage and apoptosis in hippocampal neurons.
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