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作 者:马来记[1] 高树君[1] 厉保秋[1] 闫风琴 孙克任[1]
机构地区:[1]山东医科大学毒理研究室
出 处:《济宁医学院学报》1995年第2期7-9,共3页Journal of Jining Medical University
摘 要:选择健康Wistar大鼠40只,随机分为4组,每组10只。静式吸入染毒,剂量分别为0、0.5、2.0和5.0mg/L丁二烯,每天4小时,每周6天,共16周。断头处死大鼠,将头迅速投入液氮内速冻,并取出脑组织,Matsumura法制各膜蛋白,Bradford法进行蛋白定量,孔雀石绿法测定无机磷(Pi).根据Pi和蛋白质的量,计算出ATPase活性(nmolPi/mg蛋白10分钟)。结果表明脑组织神经细胞膜Na+/K+-ATPase和Ca2+/Mg2+-ATPase活性增高,Neurofilamentmyosin-typeATPase活性降低。提示脑细胞代谢活跃,神经轴突轴浆转运障碍,突触传递受阻。Wistar rats(male and female)were randomly separated into four groups(10 rats each group),which were exposed respectively to air containing 0、0.5、2.0、and 5.0mg/L 1,3-butadiene in the closed system,4 hours per dey,6 days per week,for 16 weeks. The rats were killed by cutting heads off,throwing them into liquid nitrogen immediately,and extracting brains.The membrane was prepared by a modified procedure as desecibed by Matsumura.Protein determination of memerane was by the method of Bradford.Pi was determined by the method of Kwol-Ming Chan,ATPase activity(nmol Pi/mg prot 10min)ws calculated on the basis of quantities of protein and Pi.The results of this study showed that Na+/K+-ATPase and Ca2+/Mg2+-ATPase activity of brain cell membrane were raised ;neurofilament myosin-type ATPase activity was reduced.The results indicated that the metabolism of brain cells was active;the axoplasmic transport of axon was damaged;synaptic transmission function was abnormal.
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