Study of Pesticide Genotoxicity

Waters, Michael D.; Sandhu, Shahbeg S.; Simmon, Vincent F.; Mortelmans, Kristien; Mitchell, Ann D.; Jorgenson, T.A.; Jones, David; Valencia, R.; Garrett, Neil

doi:10.1007/978-1-4684-4352-3_23

Cited by 57 publications

(29 citation statements)

References 13 publications

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“…More than 1,000 chemicals have been classified as pesticides and a number of them have genotoxic properties [Tezuka et al, 1980;Waters et al, 1982;Garret et al, 1986;Sinha, 1989;IARC, 1991]. Some studies have shown a significant increased risk of lung cancer [Barthel, 1981], bladder cancer [De Ferrari et al, 1991;Viel and Chalier, 1995], and leukemia [Brown et al, 1990;Blair et al, 1992;Blair and Zahm, 1995] in workers exposed to pesticides.…”

Section: Introductionmentioning

confidence: 98%

Biomonitoring with the comet assay of Greek greenhouse workers exposed to pesticides

Piperakis

Petrakou

Tsilimigaki

et al. 2003

Environ and Mol Mutagen

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The pesticides in use in Greek greenhouses include a number of agents known to be mutagens and carcinogens. In the present study, we evaluated whether occupational exposure of agricultural workers to a complex mixture of pesticides resulted in a significant increase in DNA damage in human peripheral blood lymphocytes (PBLs). A total of 116 healthy individuals were divided into groups based on exposure to pesticides, smoking status, and gender. Alkaline comet assays performed on PBLs from these individuals indicated no statistically significant differences in basal DNA damage between the study groups. In addition, exposure of PBLs to a dose of hydrogen peroxide led to a similar degree of DNA damage and subsequent repair for all the study populations. The results of the study indicate that the agricultural workers who participated in this study had no detectable increase in DNA damage or alteration in the cellular response to DNA damage.

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Section: Introductionmentioning

confidence: 98%

Biomonitoring with the comet assay of Greek greenhouse workers exposed to pesticides

Piperakis

Petrakou

Tsilimigaki

et al. 2003

Environ and Mol Mutagen

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“…When mutagenic activity was assessed in bacterial systems either positive or negative results have been reported. Carbofuran has been found to be non-mutagenic in Salmonella typhimurium since negative or weak positive response were observed in the number of mitotic recombinants regardless of the presence or absence of a rat liver metabolic activation system (Blevins et al, 1977a;Gentile et al, 1982;Waters et al, 1982;Haworth & Lawlor, 1983;Hour et al, 1998;Yoon et al, 2001). These results indicate that carbofuran cannot be considered mutagenic in bacterial systems.…”

Section: Carbofuran Genotoxicity and Cytotoxicity Profilesmentioning

confidence: 99%

Genetic Toxicological Profile of Carbofuran and Pirimicarb Carbamic Insecticides

Soloneski¹,

Larramendy²

2012

Insecticides - Pest Engineering

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“…The genotoxic activity of acephate revealed highly contradictory results. It has mutagenic activity and has been shown to produce gene mutation, chromosomal alteration, micronuclei (MN) and dominant lethality in prokaryotes and eukaryotes, and in mammalian cells including human and monkey lymphocytes, mouse lymphoma cells, CHO cells, and murine bone marrow cells (Simmon et al 1978;Waters et al 1982;Jones et al 1984;Carver et al 1985;Behera and Bhunya 1989;Jena and Bhunya 1994;Hour et al 1998). In addition, Das et al (2006) reported that acephate induced apoptosis and necrosis in cultured human peripheral blood lymphocytes in in vitro conditions using the DNA diffusion assay.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the cytogenetic damage induced by the organophosphorous insecticide acephate

et al. 2009

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The organophosphorous insecticide acephate was tested for its ability to induce in vitro cytogenetic effect in human peripheral lymphocytes by using the chromosomal aberrations (CAs), sister chromatid exchange (SCE) and micronuclei (MN) assay. The level of nuclear DNA damage of acephate was evaluated by using the comet assay. Concentrations of 12.5, 25, 50, 100 and 200 lg mL -1 of acephate were used. All concentrations of acephate induced significant increase in the frequency of CAs and in the formation of MN dose dependently (r = 0.92 at 24 h, r = 0.95 at 48 h for CAs, r = 0.87 for MN). A significant increase was observed in induction of SCE at 50, 100 and 200 lg mL -1 concentrations during 24 h treatment and at all concentrations (except 12.5 lg mL -1 ) during 48 h treatment period in a dose-dependent manner (r = 0.84 at 24 h, r = 0.88 at 48 h). Acephate did not affect the replicative index and cytokinesis-block proliferation index (CBPI). However, it significantly decreased the mitotic index at all three highest concentrations (50, 100, 200 lg mL -1 ) for 24 h treatment and at all concentrations (except 12.5 lg mL -1 ) for 48 h treatment, dose-dependently (r = 0.94 at 24 h, r = 0.92 at 48 h). A significant increase in mean comet tail length was observed at 100 and 200 lg mL -1 concentrations compared with negative control in a concentration-dependent manner (r = 0.94). The mean comet tail intensity was significantly increased at only 200 lg mL -1 concentration. The present results indicate that acephate is a clastogenic, cytotoxic agent and it causes DNA damage at high concentrations in human lymphocytes in culture.

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Study of Pesticide Genotoxicity

Cited by 57 publications

References 13 publications

Biomonitoring with the comet assay of Greek greenhouse workers exposed to pesticides

Biomonitoring with the comet assay of Greek greenhouse workers exposed to pesticides

Genetic Toxicological Profile of Carbofuran and Pirimicarb Carbamic Insecticides

Evaluation of the cytogenetic damage induced by the organophosphorous insecticide acephate

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