Cytogenetic damage and induction of pro-oxidant state in human lymphocytes exposed in vitro to gliphosate, vinclozolin, atrazine, and DPX-E9636

Lioi, Maria Brigida; Scarfì, Maria Rosaria; Santoro, Antonietta; Barbieri, Rocchina; Zeni, Olga; Salvemini, Francesca; Berardino, D. Di; Ursini, Matilde Valeria

doi:10.1002/(sici)1098-2280(1998)32:1<39::aid-em5>3.0.co;2-6

Cited by 66 publications

(51 citation statements)

References 32 publications

(6 reference statements)

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“…Because this specific biologic pathway operates only in plants and microorganisms, the mechanism is not considered to be a risk for humans. Nevertheless, genotoxic, hormonal, and enzymatic effects of glyphosate in mammals have been reported [20, 22–25]. In rats, glyphosate was found to decrease the activity of some detoxifying enzymes, cytochrome P-450, and monooxygenase activities and the intestinal activity of aryl hydrocarbon hydroxylase when injected into the abdomen [26].…”

Section: Introductionmentioning

confidence: 99%

Clastogenic Effects of Glyphosate in Bone Marrow Cells of Swiss Albino Mice

Prasad

Srivastava

Singh

et al. 2009

Journal of Toxicology

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Glyphosate (N-(phosphonomethyl) glycine, C3H8NO5P), a herbicide, used to control unwanted annual and perennial plants all over the world. Nevertheless, occupational and environmental exposure to pesticides can pose a threat to nontarget species including human beings. Therefore, in the present study, genotoxic effects of the herbicide glyphosate were analyzed by measuring chromosomal aberrations (CAs) and micronuclei (MN) in bone marrow cells of Swiss albino mice. A single dose of glyphosate was given intraperitoneally (i.p) to the animals at a concentration of 25 and 50 mg/kg b.wt. Animals of positive control group were injected i.p. benzo(a)pyrene (100 mg/kg b.wt., once only), whereas, animals of control (vehicle) group were injected i.p. dimethyl sulfoxide (0.2 mL). Animals from all the groups were sacrificed at sampling times of 24, 48, and 72 hours and their bone marrow was analyzed for cytogenetic and chromosomal damage. Glyphosate treatment significantly increases CAs and MN induction at both treatments and time compared with the vehicle control (P < .05). The cytotoxic effects of glyphosate were also evident, as observed by significant decrease in mitotic index (MI). The present results indicate that glyphosate is clastogenic and cytotoxic to mouse bone marrow.

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Section: Introductionmentioning

confidence: 99%

Clastogenic Effects of Glyphosate in Bone Marrow Cells of Swiss Albino Mice

Prasad

Srivastava

Singh

et al. 2009

Journal of Toxicology

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“…Glyphosate did not show any genotoxic activity in a battery of assays (Garry et al 1999; Grisolia 2002; Li and Long 1988; Wildeman and Nazar 1982). However, other studies observed that glyphosate treatment of human lymphocytes in vitro resulted in increased sister chromatid exchanges (Bolognesi et al 1997), chromosomal aberrations (Lioi et al 1998b), and indicators of oxidative stress (Lioi et al 1998b). Some studies found slightly greater toxicity of the Roundup formulation compared with glyphosate, in terms of both acute toxicity (Folmar et al 1979; Martinez et al 1990; Mitchell et al 1987) and genotoxicity (Bolognesi et al 1997; Vigfusson and Vyse 1980).…”

mentioning

confidence: 99%

“…Because this specific biologic pathway operates only in plants and microorganisms, the mechanism is not considered to be a risk for humans. Nevertheless, genotoxic, hormonal, and enzymatic effects in mammals have been reported (Bolognesi et al 1997; Daruich et al 2001; El Demerdash et al 2001; Hietanen et al 1983; Lioi et al 1998a, 1998b; Olorunsogo et al 1979; Peluso et al 1998; Walsh et al 2000; Yousef et al 1995). …”

mentioning

confidence: 99%

Cancer Incidence among Glyphosate-Exposed Pesticide Applicators in the Agricultural Health Study

Roos

Blair²,

Rusiecki³

et al. 2005

Environ Health Perspect

222

257

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Glyphosate is a broad-spectrum herbicide that is one of the most frequently applied pesticides in the world. Although there has been little consistent evidence of genotoxicity or carcinogenicity from in vitro and animal studies, a few epidemiologic reports have indicated potential health effects of glyphosate. We evaluated associations between glyphosate exposure and cancer incidence in the Agricultural Health Study (AHS), a prospective cohort study of 57,311 licensed pesticide applicators in Iowa and North Carolina. Detailed information on pesticide use and other factors was obtained from a self-administered questionnaire completed at time of enrollment (1993–1997). Among private and commercial applicators, 75.5% reported having ever used glyphosate, of which > 97% were men. In this analysis, glyphosate exposure was defined as a) ever personally mixed or applied products containing glyphosate; b) cumulative lifetime days of use, or “cumulative exposure days” (years of use × days/year); and c) intensity-weighted cumulative exposure days (years of use × days/year × estimated intensity level). Poisson regression was used to estimate exposure–response relations between glyphosate and incidence of all cancers combined and 12 relatively common cancer subtypes. Glyphosate exposure was not associated with cancer incidence overall or with most of the cancer subtypes we studied. There was a suggested association with multiple myeloma incidence that should be followed up as more cases occur in the AHS. Given the widespread use of glyphosate, future analyses of the AHS will allow further examination of long-term health effects, including less common cancers.

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“…As the identification of copy number variation within the zebrafish genome has been completed (Brown et al, 2012), this initial assessment utilized zebrafish fibroblast cells for the study of CNA formation following atrazine exposure to eliminate detection of copy number variants that would be present among different individual fish. The genotoxicity of atrazine has been under investigation and has produced conflicting results which have ranged from evidence of no genotoxicity (Kligerman et al, 2000a; Surrallés et al, 1995; Zeljezic et al, 2006), to the generation of chromosomal aberrations (CA), sister chromatid exchanges (SEC), and increases in coefficient of variation (CV) at various dose levels and exposure periods (Biradar and Rayburn, 1995; Lioi et al, 1998; Rayburn et al, 2001; Taets et al, 1998). …”

Section: Discussionmentioning

confidence: 99%

“…The majority of in vitro studies have been conducted in Chinese hamster ovary (CHO) and human lymphocyte cells. Positive studies indicate that atrazine elicits genotoxicity through chromosomal aberrations (CA), sister chromatid exchanges (SCEs), and increases in the coefficient of variation (CV) at a variety of concentrations and exposure periods (Biradar and Rayburn, 1995; Lioi et al, 1998; Rayburn et al, 2001; Taets et al, 1998). While contrasting studies do not demonstrate any significant genotoxicity (Dunkelberg et al, 1994; Kligerman et al, 2000a, 2000b; Roloff et al, 1992; Surrallés et al, 1995; Zeljezic et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Atrazine exposure elicits copy number alterations in the zebrafish genome

Wirbisky

Freeman

2017

Comparative Biochemistry and Physiology Part C: Toxicology &

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Atrazine is an agricultural herbicide used throughout the Midwestern United States that frequently contaminates potable water supplies resulting in human exposure. Using the zebrafish model system, an embryonic atrazine exposure was previously reported to decrease spawning rates with an increase in progesterone and ovarian follicular atresia in adult females. In addition, alterations in genes associated with distinct molecular pathways of the endocrine system were observed in brain and gonad tissue of the adult females and males. Current hypotheses for mechanistic changes in the developmental origins of health and disease include genetic (e.g., copy number alterations) or epigenetic (e.g., DNA methylation) mechanisms. As such, in the current study we investigated whether an atrazine exposure would generate copy number alterations (CNAs) in the zebrafish genome. A zebrafish fibroblast cell line was used to limit detection to CNAs caused by the chemical exposure. First, cells were exposed to a range of atrazine concentrations and a crystal violet assay was completed, showing confluency decreased by ∼60% at 46.3 μM. Cells were then exposed to 0, 0.463, 4.63, or 46.3 μM atrazine and array comparative genomic hybridization completed. Results showed 34, 21, and 44 CNAs in the 0.463, 4.63, and 46.3μM treatments, respectively. Furthermore, CNAs were associated with previously reported gene expression alterations in adult male and female zebrafish. This study demonstrates that atrazine exposure can generate CNAs that are linked to gene expression alterations observed in adult zebrafish exposed to atrazine during embryogenesis providing a mechanism of the developmental origins of atrazine endocrine disruption.

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Cytogenetic damage and induction of pro-oxidant state in human lymphocytes exposed in vitro to gliphosate, vinclozolin, atrazine, and DPX-E9636

Cited by 66 publications

References 32 publications

Clastogenic Effects of Glyphosate in Bone Marrow Cells of Swiss Albino Mice

Clastogenic Effects of Glyphosate in Bone Marrow Cells of Swiss Albino Mice

Cancer Incidence among Glyphosate-Exposed Pesticide Applicators in the Agricultural Health Study

Atrazine exposure elicits copy number alterations in the zebrafish genome

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