Disruption of Intracellular ATP Generation and Tight Junction Protein Expression during the Course of Brain Edema Induced by Subacute Poisoning of 1,2-Dichloroethane

亚急性1,2-二氯乙烷中毒诱发脑水肿过程中细胞内ATP生成和紧密连接蛋白表达的紊乱

阅读:1

Abstract

The aim of this study was to explore changes in intracellular ATP generation and tight junction protein expression during the course of brain edema induced by subacute poisoning of 1,2-dichloroethane (1,2-DCE). Mice were exposed to 1.2 g/m(3) 1,2-DCE for 3.5 h per day for 1, 2, or 3 days, namely group A, B, and C. Na(+)-K(+)-ATPase and Ca(2+)-ATPase activity, ATP and lactic acid content, intracellular free Ca(2+) concentration and ZO-1 and occludin expression in the brain were measured. Results of present study disclosed that Ca(2+)-ATPase activities in group B and C, and Na(+)/K(+)-ATPase activity in group C decreased, whereas intracellular free Ca(2+) concentrations in group B and C increased significantly compared with control. Moreover, ATP content decreased, whereas lactic acid content increased significantly in group C compared with control. On the other hand, expressions of ZO-1 and occludin at both the protein and gene levels in group B and C decreased significantly compared with control. In conclusion, findings from this study suggest that calcium overload and depressed expression of tight junction associated proteins, such as ZO-1 and occludin might play an important role in the early phase of brain edema formation induced by subacute poisoning of 1,2-DCE.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。