DNA damage and mutagenicity induced by endosulfan and its metabolites

Bajpayee, M; Pandey, AK; Zaidi, S; Musarrat, J; Parmar, D; Mathur, N; Seth, PK; Dhawan, A

HERO ID

677399

Reference Type

Journal Article

Year

2006

Language

English

PMID

16933317

HERO ID 677399
In Press No
Year 2006
Title DNA damage and mutagenicity induced by endosulfan and its metabolites
Authors Bajpayee, M; Pandey, AK; Zaidi, S; Musarrat, J; Parmar, D; Mathur, N; Seth, PK; Dhawan, A
Journal Environmental and Molecular Mutagenesis
Volume 47
Issue 9
Page Numbers 682-692
Abstract Endosulfan is a widely used broad-spectrum organochlorine pesticide, which acts as a contact and stomach poison. Nontarget species, such as cattle, fish, birds, and even humans, are also affected. Studies on the genotoxicity and mutagenicity of endosulfan have been inconsistent and nothing is known about the genotoxicity of its metabolites. In the present study, endosulfan (as a commercial isomeric mixture and as the alpha- and beta-isomers), and metabolites of endosulfan (the sulfate, lactone, ether, hydroxyether, and diol derivatives) were assayed for their ability to induce DNA damage in Chinese hamster ovary (CHO) cells and human lymphocytes using the Comet assay and were assayed for their mutagenicity using the Salmonella reversion assay (Ames test with TA98, TA97a, TA102, TA104, and TA100, with and without S9 activation). The compounds produced statistically significant (P < 0.01), concentration-dependent (0.25-10 microM) increases in DNA damage in both CHO cells and human lymphocytes. Endosulfan lactone caused the most DNA damage in CHO cells, while the isomeric mixture of endosulfan produced the greatest response in lymphocytes. The test compounds also were mutagenic in Salmonella strains at concentrations of 1-20 mug/plate (P < 0.05), with TA98 being the most sensitive strain and the diol and hydroxyether metabolites producing the highest responses. The results indicate that exposure to sublethal doses of endosulfan and its metabolites induces DNA damage and mutation. The contribution of the metabolites to the genotoxicity of the parent compound in Salmonella and mammalian cells, however, is unclear, and the pathways leading to bacterial mutation and mammalian cell DNA damage appear to differ.
Doi 10.1002/em.20255
Pmid 16933317
Wosid WOS:000242773100007
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword Animals; CHO Cells; Cell Survival/drug effects; Comet Assay; Cricetinae; Cricetulus; DNA Damage; Endosulfan/metabolism/ toxicity; Humans; Insecticides/metabolism/ toxicity; Lymphocytes; Male; Mutagens/metabolism/ toxicity; Salmonella typhimurium/drug effects
Is Qa No