Document Detail

Dichlorvos-induced cell cycle arrest and DNA damage repair activation in primary rat microglial cells.
MedLine Citation:
PMID:  23280485     Owner:  NLM     Status:  Publisher    
Dichlorvos, an organophosphate (OP), is known to cause oxidative stress in the central nervous system (CNS). Previously we have shown that dichlorvos treatment promoted the levels of proinflammatory molecules and ultimately induced apoptotic cell death in primary microglial cells. Here we studied the effect of dichlorvos on crucial cell cycle regulatory proteins and the DNA damage sensor ataxia-telangiectasia mutated (ATM). We found a significant increase in p53 and its downstream target, p21, levels in dichlorvos-treated microglial cells compared with control cells. Moreover, dichlorvos exposure promoted the levels of different cell cycle regulatory proteins. These results along with flow cytometry results suggested that primary microglial cells were arrested at G1 and G2/M phase after dichlorvos exposure. We have shown in a previous study that dichlorvos can induce DNA damage in microglia; here we found that microglial cells also tried to repair this damage by inducing a DNA repair enzyme, i.e., ATM. We observed a significant increase in the levels of ATM after dichlorvos treatment compared with control. © 2012 Wiley Periodicals, Inc.
Aditya Sunkaria; Willayat Yousuf Wani; Deep Raj Sharma; Kiran Dip Gill
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-12-26
Journal Detail:
Title:  Journal of neuroscience research     Volume:  -     ISSN:  1097-4547     ISO Abbreviation:  J. Neurosci. Res.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2013-1-2     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7600111     Medline TA:  J Neurosci Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
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