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

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 gro...

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Autores principales: Wang, Gaoyang, Yuan, Yuan, Gao, Lanyue, Tan, Xiaoqiong, Yang, Guangqian, Zhao, Fenghong, Jin, Yaping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5787108/
https://www.ncbi.nlm.nih.gov/pubmed/29410610
http://dx.doi.org/10.3389/fnins.2018.00012
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author Wang, Gaoyang
Yuan, Yuan
Gao, Lanyue
Tan, Xiaoqiong
Yang, Guangqian
Zhao, Fenghong
Jin, Yaping
author_facet Wang, Gaoyang
Yuan, Yuan
Gao, Lanyue
Tan, Xiaoqiong
Yang, Guangqian
Zhao, Fenghong
Jin, Yaping
author_sort Wang, Gaoyang
collection PubMed
description 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.
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spelling pubmed-57871082018-02-06 Disruption of Intracellular ATP Generation and Tight Junction Protein Expression during the Course of Brain Edema Induced by Subacute Poisoning of 1,2-Dichloroethane Wang, Gaoyang Yuan, Yuan Gao, Lanyue Tan, Xiaoqiong Yang, Guangqian Zhao, Fenghong Jin, Yaping Front Neurosci Neuroscience 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. Frontiers Media S.A. 2018-01-23 /pmc/articles/PMC5787108/ /pubmed/29410610 http://dx.doi.org/10.3389/fnins.2018.00012 Text en Copyright © 2018 Wang, Yuan, Gao, Tan, Yang, Zhao and Jin. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Wang, Gaoyang
Yuan, Yuan
Gao, Lanyue
Tan, Xiaoqiong
Yang, Guangqian
Zhao, Fenghong
Jin, Yaping
Disruption of Intracellular ATP Generation and Tight Junction Protein Expression during the Course of Brain Edema Induced by Subacute Poisoning of 1,2-Dichloroethane
title Disruption of Intracellular ATP Generation and Tight Junction Protein Expression during the Course of Brain Edema Induced by Subacute Poisoning of 1,2-Dichloroethane
title_full Disruption of Intracellular ATP Generation and Tight Junction Protein Expression during the Course of Brain Edema Induced by Subacute Poisoning of 1,2-Dichloroethane
title_fullStr Disruption of Intracellular ATP Generation and Tight Junction Protein Expression during the Course of Brain Edema Induced by Subacute Poisoning of 1,2-Dichloroethane
title_full_unstemmed Disruption of Intracellular ATP Generation and Tight Junction Protein Expression during the Course of Brain Edema Induced by Subacute Poisoning of 1,2-Dichloroethane
title_short Disruption of Intracellular ATP Generation and Tight Junction Protein Expression during the Course of Brain Edema Induced by Subacute Poisoning of 1,2-Dichloroethane
title_sort disruption of intracellular atp generation and tight junction protein expression during the course of brain edema induced by subacute poisoning of 1,2-dichloroethane
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5787108/
https://www.ncbi.nlm.nih.gov/pubmed/29410610
http://dx.doi.org/10.3389/fnins.2018.00012
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