Brain cholinergic, behavioral, and morphological development in rats exposed in utero to methylparathion

Gupta, Ramesh C.; Rech, Richard H.; Lovell, Kathryn L.; Welsch, Frank; Thornburg, John E.

doi:10.1016/0041-008x(85)90180-2

Cited by 87 publications

(26 citation statements)

References 26 publications

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“…Toxicologic studies have shown that OP compounds can cross the placental and blood-brain barriers (Chanda and Pope 1996;Gupta et al 1985;Muto et al 1992). As part of a prospective cohort study being conducted by the Columbia Center for Children's Environmental Health, Whyatt et al (2003) analyzed 142 paired blood samples collected at birth from minority mothers and newborns for 29 pesticides.…”

Section: Discussionmentioning

confidence: 99%

Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort.

Castorina

Bradman

McKone

et al. 2003

Environ Health Perspect

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Approximately 230,000 kg of organophosphate (OP) pesticides are applied annually in California's Salinas Valley. These activities have raised concerns about exposures to area residents. We collected three spot urine samples from pregnant women (between 1999 and 2001) enrolled in CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas), a longitudinal birth cohort study, and analyzed them for six dialkyl phosphate metabolites. We used urine from 446 pregnant women to estimate OP pesticide doses with two deterministic steady-state modeling methods: method 1, which assumed the metabolites were attributable entirely to a single diethyl or dimethyl OP pesticide; and method 2, which adapted U.S. Environmental Protection Agency (U.S. EPA) draft guidelines for cumulative risk assessment to estimate dose from a mixture of OP pesticides that share a common mechanism of toxicity. We used pesticide use reporting data for the Salinas Valley to approximate the mixture to which the women were exposed. Based on average OP pesticide dose estimates that assumed exposure to a single OP pesticide (method 1), between 0% and 36.1% of study participants' doses failed to attain a margin of exposure (MOE) of 100 relative to the U.S. EPA oral benchmark dose(10) (BMD(10)), depending on the assumption made about the parent compound. These BMD(10) values are doses expected to produce a 10% reduction in brain cholinesterase activity compared with background response in rats. Given the participants' average cumulative OP pesticide dose estimates (method 2) and regardless of the index chemical selected, we found that 14.8% of the doses failed to attain an MOE of 100 relative to the BMD(10) of the selected index. An uncertainty analysis of the pesticide mixture parameter, which is extrapolated from pesticide application data for the study area and not directly quantified for each individual, suggests that this point estimate could range from 1 to 34%. In future analyses, we will use pesticide-specific urinary metabolites, when available, to evaluate cumulative OP pesticide exposures.

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Section: Discussionmentioning

confidence: 99%

Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort.

Castorina

Bradman

McKone

et al. 2003

Environ Health Perspect

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“…Another group that carried out extensive analyses observed in rats what they called ''subtle alterations in selected behaviors of the offspring.' ' Gupta et al [1985] administered the OP methyl parathion from gestation days 6-20. Their oral doses elicited no (1.0 mg/kg) or minimal (1.5 mg/kg) cholinergic signs such as excessive salivation.…”

Section: Animal Modelsmentioning

confidence: 99%

Pesticides as a source of developmental disabilities

Weiss

1997

Ment. Retard. Dev. Disabil. Res. Rev.

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“…MP was found to be teratogenic in chicken embryos and rodents in which it induced fetal mortality and skeletal malformations such as cleft palate and cervical ribs (Jelinek et al, 1985;Vernagy and Deli, 1985;IPCS, 1993;Kumar and Devi, 1992). Daily intra-peritoneal injections of 1 or 1.5 mg/kg MP to pregnant rats during gestation Days 6-19 induced a decrease in fetal and maternal protein synthesis in a dose-dependent manner (Gupta et al, 1984) and also decreased the postnatal cholinesterase levels (Gupta et al, 1985). At dose-levels of 2.5 -5 mg/kg, MP decreased compensatory ovary weight gain and incidences of healthy follicles in hemi-castrated rats (Dhondup and Kaliwal, 1997), and also affected the estrous cycle (Asmathbanu and Kaliwal, 1997).…”

Section: Introductionmentioning

confidence: 99%

An Organophosphate Insecticide Methyl Parathion (O- O- Dimethyl O-4-Nitrophenyl Phosphorothioate) Induces Cytotoxic Damage and Tubular Atrophy in the Testis Despite Elevated Testosterone Level in the Rat

Narayana

Prashanthi²,

Arunkumar³

et al. 2006

J. Toxicol. Sci.

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-Methyl parathion (MP) is an organophosphate pesticide used in agriculture, although quite often illegally used indoors to contain insects. The present study was planned to investigate the effects of MP on rat testis. Adult male Wistar rats (13-14 weeks) were treated with MP as follows. Experiment 1-0, 1.75, 3.5 or 7 mg/kg i.p. for 5 days and sacrificed on Day 14; experiment 2 and 3-0, 0.5, or 1 mg/kg i.p. for 12 days, and sacrificed on Days 130 and 77, respectively; experiment 4-0, 0.75, or 1.5 mg/kg i.p. for 25 days, and sacrificed on Day 17; experiment 5-0 or 3.5 mg/kg po for 25 days, and sacrificed on Day 17, after the last exposure. MP decreased the body weight and the testis weight in experiments 4 and 5 (p<0.05-0.001) due to decreased food intake and tubular atrophy respectively. MP increased the intra-testicular testosterone level and decreased the LH level in experiments 4 and 5. The seminiferous epithelium showed sloughing of germ cells, vacuoles, focal necrosis, and formation of multinucleated giant cells, cellular degeneration (nuclear pyknosis, halo appearance and shrinkage of nuclei) and tubular atrophy, especially in experiment 4. The degree of testicular damage was higher in experiment 4>5>1>3>2 indicating more effect of prolonged i.p. treatment. Homogenization-resistant spermatid count was decreased in experiments 1, 4 and 5, and MP also decreased the tubular diameter, and epithelial height (p<0.05-0.001). Incidences of stage XIV tubules, number of meiotic figures and elongating spermatids were also decreased, whereas the incidence of tubules showing epithelial sloughing increased (p<0.05-0.001). We conclude that MP is a reproductive toxicant in male rats which causes significant testicular damage in the testis.

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Brain cholinergic, behavioral, and morphological development in rats exposed in utero to methylparathion

Cited by 87 publications

References 26 publications

Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort.

Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort.

Pesticides as a source of developmental disabilities

An Organophosphate Insecticide Methyl Parathion (O- O- Dimethyl O-4-Nitrophenyl Phosphorothioate) Induces Cytotoxic Damage and Tubular Atrophy in the Testis Despite Elevated Testosterone Level in the Rat

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