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Mechanism of Pyrethroid Pesticide-Induced Apoptosis: Role of Calpain and the ER Stress Pathway.
MedLine Citation:
PMID:  21555338     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Exposure to the pyrethroid pesticide deltamethrin has been demonstrated to cause apoptosis both in vitro and in vivo. However, the molecular pathways leading to deltamethrin-induced apoptosis have not been established. To identify these pathways, SK-N-AS neuroblastoma cells were exposed to deltamethrin (100 nM-5 μM) for 24-48 hrs. Deltamethrin produced a time and dose-dependent increase (21-121%) in DNA fragmentation, an indicator of apoptosis. Data demonstrate that the initiation of DNA fragmentation resulted from interaction of deltamethrin with Na(+) channels and consequent calcium influx, as tetrodotoxin and the intracellular Ca(2+) chelator BAPTA-AM completely prevented apoptosis. DNA fragmentation was accompanied by increased caspase-9 and 3 activities, and was abolished by specific caspase-9 and 3 inhibitors. However, deltamethrin did not increase cytosolic cytochrome c levels, indicating that the mitochondrial pathway was likely not involved. Additional studies demonstrated that deltamethrin exposure activated caspase-12 activity, and that pharmacological inhibition and siRNA knockdown of calpain, prevented deltamethrin-induced DNA fragmentation, thus indicating a role for the ER stress pathway. This was confirmed by the observation that inhibition of eIF2α abolished deltamethrin-induced DNA fragmentation. Together, these data demonstrate that deltamethrin causes apoptosis through its interaction with Na(+) channels, leading to calcium overload and activation of the ER stress pathway. Because ER stress and the subsequent unfolded protein response have been observed in a number of neurodegenerative diseases, these data provide mechanistic information by which high level exposure to pyrethroids may contribute to neurodegeneration.
Authors:
Muhammad M Hossain; Jason R Richardson
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-5-9
Journal Detail:
Title:  Toxicological sciences : an official journal of the Society of Toxicology     Volume:  -     ISSN:  1096-0929     ISO Abbreviation:  -     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-5-10     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9805461     Medline TA:  Toxicol Sci     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Environmental and Occupational Medicine, Robert Wood Johnson Medical School, and Environmental and Occupational Health Sciences Institute, Piscataway, NJ 08854, USA.
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