Abstract
This study was designed to explore the role of cytochrome P4502E1 (CYP2E1) expression in the course of brain edema induced by subacute poisoning with 1,2-dichloroethane (1,2-DCE). Mice were randomly divided into five groups: the control group, the 1,2-DCE poisoned group, and the low-, medium- and high-dose diallyl sulfide (DAS) intervention groups. The present study found that CYP2E1 expression levels in the brains of the 1,2-DCE-poisoned group were upregulated transcriptionally; in contrast, the levels were suppressed by DAS pretreatment in the intervention groups. In addition, the expression levels of both Nrf2 and HO-1 were also upregulated transcriptionally in the brains of the 1,2-DCE-poisoned group, while they were suppressed dose-dependently in the intervention groups. Moreover, compared with the control group, MDA levels and water contents in the brains of the 1,2-DCE-poisoned group increased, whereas NPSH levels and tight junction (TJ) protein levels decreased significantly. Conversely, compared with the 1,2-DCE- poisoned group, MDA levels and water contents in the brains of the intervention groups decreased, and NPSH levels and TJ protein levels increased significantly. Furthermore, pathological changes of brain edema observed in the 1,2-DCE-poisoned group were markedly improved in the intervention groups. Collectively, our results suggested that CYP2E1 expression could be transcriptionally upregulated in 1,2-DCE-poisoned mice, which might enhance 1,2-DCE metabolism in vivo, and induce oxidative damage and TJ disruption in the brain, ultimately leading to brain edema.
Highlights
The synthetic halocarbon 1,2-dichloroethane (1,2-DCE, CAS number: 107-06-2) is widely manufactured around the world and is used primarily in the production of vinyl chloride (Yu et al, 2013; Sun et al, 2016). 1,2-DCE is a colorless and volatile organic liquid; it is used as a general organic solvent in China and other countries
The body weights of mice in the poisoned group and the intervention groups decreased significantly at the end of the 3-day exposure compared with the control group
The present study found that cytochrome P4502E1 (CYP2E1) expression in the brains of 1,2-DCE-poisoned mice was upregulated transcriptionally and that pretreatment of 1,2-DCE-poisoned mice with diallyl sulfide (DAS) could efficiently suppress the enhanced expression of CYP2E1
Summary
The synthetic halocarbon 1,2-dichloroethane (1,2-DCE, CAS number: 107-06-2) is widely manufactured around the world and is used primarily in the production of vinyl chloride (Yu et al, 2013; Sun et al, 2016). 1,2-DCE is a colorless and volatile organic liquid; it is used as a general organic solvent in China and other countries. 1,2-DCE is a colorless and volatile organic liquid; it is used as a general organic solvent in China and other countries. It can be evaporated quickly into the air when 1,2-DCE is used as a thinner of industrial adhesives, as a consequence, workers may inhale high. CYP2E1 in 1,2-Dichloroethane Induced Brain Edema vapor concentrations of 1,2-DCE in the workplace. Accumulated evidence has found that exposure to high concentrations of 1,2DCE through the air could cause acute and subacute poisoning in both workers and laboratory animals (Hotchkiss et al, 2010; Wang et al, 2014; Zhou et al, 2015). Our understanding in relation to the mechanisms of 1,2-DCE-induced brain edema is limited
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
