Document Detail


Malathion-induced oxidative stress, cytotoxicity, and genotoxicity in human liver carcinoma (HepG2) cells.
MedLine Citation:
PMID:  19399848     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Malathion is an organophosphate pesticide that is known for its high toxicity to insects and low to moderate potency to humans and other mammals. Its toxicity has been associated with the inhibition of acetylcholinesterase activity, leading to the interference with the transmission of nerve impulse, accumulation of acetylcholine at synaptic junctions, and subsequent induction of adverse health effects including headache, dizziness, nausea, vomiting, bradycardia, and miosis. Oxidative stress (OS) has been reported as a possible mechanism of malathion toxicity in humans. Hence, the aim of this study was to examine the role of OS in malathion-induced cytotoxicity and genotoxicity. To achieve this goal, MTT, lipid peroxidation, and single cell gel electrophoresis (Comet) assays were performed, respectively, to evaluate the levels of cell viability, malondialdehyde (MDA) production, and DNA damage in human liver carcinoma (HepG(2)) cells. Study results indicated that malathion is mitogenic at lower levels of exposure, and cytotoxic at higher levels of exposure. Upon 48 h of exposure, the average percentages of cell viability were 100% +/- 11%, 117% +/- 15%, 86% +/- 15%, 35% +/- 9%, and 27% +/- 7% for 0, 6, 12, 18, and 24 mM, respectively. In the lipid peroxidation assay, the concentrations of MDA produced were 12.55 +/- 0.16, 20.65 +/- 0.27, 31.1 +/- 0.40, 34.75 +/- 0.45, and 15.1 +/- 0.20 muM in 0, 6, 12, 18, and 24 mM malathion, respectively. The Comet assay showed a significant increase in DNA damage at the 24 mM malathion exposure. Taken together, our results indicate that malathion exposure at higher concentrations induces cytotoxic and genotoxic effects in HepG(2) cells, and its toxicity may be mediated through OS as evidenced by a significant production of MDA, an end product of lipid peroxidation.
Authors:
Pamela D Moore; Clement G Yedjou; Paul B Tchounwou
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Environmental toxicology     Volume:  25     ISSN:  1522-7278     ISO Abbreviation:  Environ. Toxicol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-03     Completed Date:  2010-07-23     Revised Date:  2013-07-22    
Medline Journal Info:
Nlm Unique ID:  100885357     Medline TA:  Environ Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  221-6     Citation Subset:  IM    
Copyright Information:
(c) 2009 Wiley Periodicals, Inc.
Affiliation:
Molecular Toxicology Research Laboratory, NIH RCMI, Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, 1400 Lynch Street, Jackson, MS 39217, USA.
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MeSH Terms
Descriptor/Qualifier:
Cell Culture Techniques
Cell Survival / drug effects
Comet Assay
DNA Damage*
Dose-Response Relationship, Drug
Hep G2 Cells
Humans
Lipid Peroxidation / drug effects
Malathion / toxicity*
Malondialdehyde / metabolism
Mutagens / toxicity*
Oxidative Stress / drug effects*
Pesticides / toxicity*
Grant Support
ID/Acronym/Agency:
2G12RR13459-11/RR/NCRR NIH HHS; G12 RR013459/RR/NCRR NIH HHS; G12 RR013459-12/RR/NCRR NIH HHS; G12 RR013459-125442/RR/NCRR NIH HHS; P20 RR016476/RR/NCRR NIH HHS; P20 RR016476-049004/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Mutagens; 0/Pesticides; 121-75-5/Malathion; 542-78-9/Malondialdehyde
Comments/Corrections

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