摘要
目的探讨1,2-二氯乙烷(1,2-DCE)致大鼠急性中毒性脑病模型中细胞内钙离子的作用。方法离体培养新生SD大鼠脑皮质细胞,设对照组和1、2-DCE低、中、高剂量组,尼莫地平拮抗组。1,2-DCE终浓度分别为0.5、1.0、2.0 mmol/L,拮抗组尼莫地平终浓度为5.0 mmol/L。观察各组神经细胞超微结构、活力及细胞内钙离子浓度的变化。结果与对照组相比,高剂量组神经细胞超微结构有不同程度的损伤,各剂量组细胞活力下降(P<0.01);染毒后24 h内,随着染毒剂量的增加各剂量组细胞内钙离子浓度呈上升趋势,与对照组比较,差异有统计学意义(P<0.01);随着染毒时间的延长,低、中剂量组钙离子浓度呈单峰状,高剂量组呈双峰状;拮抗组神经细胞超微结构较高剂量组有明显改善,细胞活力高于高剂量组(P<0.01)。染毒早期和后期细胞内钙离子浓度低于高剂量组(P<0.01)。结论 1,2-DCE及其代谢产物可致神经细胞水肿坏死,随着染毒剂量的增加各染毒组细胞内钙离子浓度升高,神经细胞损伤严重程度呈上升趋势,而钙离子通道拮抗剂尼莫地平可缓解神经细胞受损程度,提示钙离子在1,2-DCE致神经细胞中毒性脑病中起到重要作用。
[Objective] To study role of calcium ions in rat model of acute intoxicated encephalopathy induced by 1,2-dichloroethane（1,2-DCE）in vitro. [Methods]The cerebral cortical cells of new born SD rats were cultured in vitro,and there were control group,three exposure groups（including low,middle and high dose group）,which were administrated with final concentrations of 1,2-DCE at 0.0,0.5,1.0,2.0 and 2.0 mmol/L,and nimodipine antagonism group（the final concentration of nimodipine was 5.0 mmol/L）. The ultrastructure and viability of nerve cells,and intracellular calcium concentration were observed.[Results]Compared with control group,there were different degrees of damage to the ultrastructure of nerve cells in high dose group,and the cell viability in three exposure groups decreased（P〈0.01）. Within 24 hours of exposure,the intracellular calcium concentrations in exposure groups increased with the increasing dose,and the difference was statistically significant between control group and exposure groups（P 〈0.01）. With increasing exposure time,the intracellular calcium concentration in low and middle dose groups showed the single peak pattern,while that in high dose group showed the bimodal pattern. The ultrastructure of nerve cells in nimodipine antagonism group improved significantly as compared with high dose group,and the cell viability was higher than that in high dose group（P〈0.01）,while the intracellular calcium concentrations during early stage and later stage were lower than those in high dose group（P〈0.01）.[Conclusion]1,2-DCE and its metabolite can lead to edema and necrosis of neurocytes.The intracellular calcium concentrations in exposure groups increase with increasing dose,while the severity of nerve cell injury shows an upward trend. The nimodipine,a calcium channel antagonist,can alleviate the damage of nerve cells,which indicates that calcium ions play an important role in acute intoxicated encephalopathy induced by1,2-DCE.
作者
王静
曹长春
WANG Jing CAO Chang-chun(Evaluation Office,Occupational Health Department,Beijing Institute of Occupational Medicine for Chemical lndustry,Beijing, 100093,China Training Department,Petroleum Occupational Health Technical Service Center of China National Petroleum Corporation,Langfang Hebei, 065000, China)
出处
《职业与健康》
CAS
2017年第1期38-40,共3页
Occupation and Health
关键词
1
2-二氯乙烷
中毒性脑病
钙离子
拮抗剂
1
2-dichloroethane
Intoxicated encephalopathy
Calcium ion
Antagonist
