劳动医学
勞動醫學
노동의학
JOURNAL OF LABOUR MEDICINE
2001年
1期
35-37
,共3页
二硫化碳%神经行为%神经组化%神经病理%分子生物技术
二硫化碳%神經行為%神經組化%神經病理%分子生物技術
이류화탄%신경행위%신경조화%신경병리%분자생물기술
[目的] 通过系列实验结果归括,评估CS2神经毒性。[方法] SD雄性大鼠吸入浓度为0、300、600、1 200和2 400 mg/m3五组,每组11~12只,4h/d,5d/周,共8周,采用神经行为、神经组化、神经病理和分子生物技术,评估CS2的神经毒性。[结果] CS2浓度为300 mg/m3可影响学习记忆和运动协调、细胞膜结构的异常、神经微丝聚集及星形胶质细胞增生、神经细胞器内质网和线粒体的溶解、细胞内外钙分布的异常、神经递质代谢和Na+-K+-ATP酶活性的变化。[结论] CS2可引起神经细胞蛋白质的共价交联结构,神经元渗透性和能量转移以及结构的影响。神经胶质酸性纤维蛋白、3-甲基-4羟基扁桃酸和某些兴奋性氨基酸(谷氨酸和门冬氨酸)可作CS2毒作用敏感标志物。
[目的] 通過繫列實驗結果歸括,評估CS2神經毒性。[方法] SD雄性大鼠吸入濃度為0、300、600、1 200和2 400 mg/m3五組,每組11~12隻,4h/d,5d/週,共8週,採用神經行為、神經組化、神經病理和分子生物技術,評估CS2的神經毒性。[結果] CS2濃度為300 mg/m3可影響學習記憶和運動協調、細胞膜結構的異常、神經微絲聚集及星形膠質細胞增生、神經細胞器內質網和線粒體的溶解、細胞內外鈣分佈的異常、神經遞質代謝和Na+-K+-ATP酶活性的變化。[結論] CS2可引起神經細胞蛋白質的共價交聯結構,神經元滲透性和能量轉移以及結構的影響。神經膠質痠性纖維蛋白、3-甲基-4羥基扁桃痠和某些興奮性氨基痠(穀氨痠和門鼕氨痠)可作CS2毒作用敏感標誌物。
[목적] 통과계렬실험결과귀괄,평고CS2신경독성。[방법] SD웅성대서흡입농도위0、300、600、1 200화2 400 mg/m3오조,매조11~12지,4h/d,5d/주,공8주,채용신경행위、신경조화、신경병리화분자생물기술,평고CS2적신경독성。[결과] CS2농도위300 mg/m3가영향학습기억화운동협조、세포막결구적이상、신경미사취집급성형효질세포증생、신경세포기내질망화선립체적용해、세포내외개분포적이상、신경체질대사화Na+-K+-ATP매활성적변화。[결론] CS2가인기신경세포단백질적공개교련결구,신경원삼투성화능량전이이급결구적영향。신경효질산성섬유단백、3-갑기-4간기편도산화모사흥강성안기산(곡안산화문동안산)가작CS2독작용민감표지물。
[Objective] This article intends to summarize the neurotoxicity of carbon disulfide(CS2) based on a sequence of experimental study. [Methods] By using a dynamic inhalation exposure system,11-12 Sprague-Dawely male rats per each group were exposed to CS2 vapor at various levels of 3,300,600,1200 and 2400 mg/m3,4h/day,5 d/week,for 8 weeks.After cessation of the exposure,a functional observation behavior (FOB) test battery was performed to assess the locomotor activity,memory and learning ability in rats;and the neurochemical,immunohistochemical,neuropathological and molecular biological techniques were employed to assess the neurotoxicological effects of CS2 in vivo and in vitro. [Results] A deficiency of neurobehavioral function,in terms of memory and learning ability,was found in the CS2-exposed group at as low as 300mg/m3 exposure level.The experimental findings indicated that CS2-induced neurotoxicity is characterized by degenerative changes of central and peripheral nervous system,which manifested as the accumulation of neurofilament,proliferation of astrocyte,dissolution of mitochodria and endoplasmic reticulum of neural organella,as well as the abnormal Ca2+ distribution and membrane structural impairment of neurons. Alterations of neurotransmitter metabolism and the activity of Na+-K+-ATP ase were also observed. [Conclusion] It is suggested that CS2 may cause cross-linking of cytoskeleton protein of neural cells,and affect the structure and permeability and energy transport of neurons. The glial fibrillary protein (GFAP),vanillylmandelic acid(VMA) and some excitatory amino acids,such as glutamic acid and aspartic acid,may be of useful biomarkers assessing the CS2-induced neurotoxicity.