Distribution and transplacental transfer of paraquat in rats and guinea-pigs

Ingebrigtsen, Kristian; Nafstad, Inger; Andersen, R.A.

doi:10.1016/0306-3623(84)90159-9

Cited by 16 publications

(6 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While effects of prenatal exposure to MPTP are equivocal, MPTP can have adverse effects after crossing the placenta into the fetus in mice and non-human primates [Weissman et al, 1989;Melamed et al, 1990;Ochi, et al, 1991;Perez-Otano et al, 1992. Likewise, PQ and DTCs are able to cross the placenta [Ingebrigsten et al, 1984;Larsson et al, 1976;Chernoff et al, 1979;Shukla et al, 2001] but effects of these compounds on the nigrostriatal DA system have not been reported.…”

Section: Introductionmentioning

confidence: 96%

A Fetal Risk Factor for Parkinson’s Disease

Barlow¹,

Richfield

Cory‐Slechta

et al. 2004

Dev Neurosci

View full text Add to dashboard Cite

A lack of strong evidence for genetic heritability of idiopathic Parkinson’s disease (PD) has focused attention on environmental toxicants in the disease etiology, particularly agrichemicals. PD is associated with advanced age, but it is unclear whether specific neuronal damage could result from insults during development. This study hypothesized that prenatal exposure to pesticides would disrupt the development of the nigrostriatal dopamine (DA) system and enhance its vulnerability to dopaminergic neurotoxicant exposures later in life. Pregnant C57BL/6J mice were treated on gestational days 10–17 with saline or the pesticides maneb (MB, 1 mg/kg) or paraquat (PQ, 0.3 mg/kg). When offspring were evaluated in adulthood, there were no significant effects of prenatal MB or PQ exposure on locomotor activity. Subsequently, offspring were treated for 8 consecutive days with saline, MB (30 mg/kg), or PQ (5 mg/kg). One week after the last exposure, only males exposed to prenatal MB and adulthood PQ showed significant reductions in locomotor activity (95%) and changes in striatal neurochemistry. Stereological assessment of the substantia nigra pars compacta (SNpc) and ventral tegmental area correspondingly confirmed selective dopaminergic-neuron loss in SNpc. The lack of changes in other exposure groups suggests a specificity to the sequence of exposures as well as gender specificity. These results suggest that prenatal exposure to MB produces selective, permanent alterations of the nigrostriatal dopaminergic system and enhances adult susceptibility to PQ exposure. This study implicates a role for developmental neurotoxicant exposure in the induction of neurodegenerative disorders such as PD.

show abstract

Section: Introductionmentioning

confidence: 96%

A Fetal Risk Factor for Parkinson’s Disease

Barlow¹,

Richfield

Cory‐Slechta

et al. 2004

Dev Neurosci

View full text Add to dashboard Cite

show abstract

“…Animal studies show that paraquat readily crosses theplacenta, where it is found in high concentrations especially in lungs, kidneys, skin, and salivary glands [7,8]. Moreover, it is demonstrated that type II pneumocytes in fetal rat lungs actively reuptake paraquat and cause tissue concentrations of the toxin to rise to levels found in adults by 2 weeks.…”

Section: Discussionmentioning

confidence: 99%

Fetal poisoning after maternal paraquat ingestion during third trimester of pregnancy: Case report and literature review

Chomchai

Tiawilai

2007

J. Med. Toxicol.

View full text Add to dashboard Cite

Introduction: Paraquat remains one of the common substances involved in intentional ingestions in Thailand. However, data on outcomes of paraquat ingestion during pregnancy is rarely available and the management is controversial.Case report: A 17-year-old female in 36ϩ weeks of gestation attempted suicide by ingesting 1/2 a glass of Gramozone™ (paraquat 27.6 % w/v) 5 hours prior to arrival to the hospital. Gastric aspiration and lavage was performed and she was given 50 g of activated charcoal and 150 g of Fuller's Earth suspension. A male infant, weighing 2,390 g with an Apgar score of 7 1 10 10 , was delivered via emergency caesarean section 7 hours after ingestion. Due to presence of paraquat in the gastric lavage fluid, the mother was placed on dexamethasone/cyclophosphamide therapy. She developed mild renal insufficiency 63 hours after the ingestion. The infant developed tachypnea immediately after birth that self-resolved. The infant developed tachypnea again on day 6 of life. A chest x-ray revealed right lower lobe infiltration that progressed to diffuse interstitial pattern; subsequent chest x-rays showed evidence of fibrosis. Both mother and infant survived and the infant was discharged and sent home with oxygen 0.5 LPM. Upon follow up at 10 months of age, he still had evidence of chronic lung disease clinically and on chest x-ray.Conclusion: Paraquat ingestion during the third trimester of pregnancy usually carries a very poor prognosis. Review of reported literature suggests that this case report represents only the second survival of mother and child.

show abstract

“…It should be pointed out that suboptimal assay conditions were reported to be at least partly responsible for the reported negative in vitro findings (Trush et al, 1981). Considering these reports and the facts that paraquat concentrates in the guinea pig and rat placenta (Ingebrigtsen el aL, 1985) and many animal studies (Bus et aL, 1975;Hoffman and Eastin, 1982;Selypes et aL, 1982;Ingebrigtsen et aL, 1985) have documented fetotoxicity of paraquat, it was viewed important to examine the response of human placental microsomes to this chemical. Redox cycling of paraquat as well as certain other chemicals and the concomitant generation of reactive oxygen species at the expense of NADPH has been proposed as the molecular mechanism of their cytotoxicity (Bus and Gibson, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…Paraquat, a widely used herbicide, is a well-known pulmonary toxicant (Smith and Heath, 1976;Haley, 1979). The reports of animal studies designed to evaluate reproductive hazards of paraquat have documented its transplacental transfer, increased embryo/fetal mortality, reduced growth rate, and high mutagenic potential (Bus et al, 1975;Hoffman and Eastin, 1982;Selypes et al, 1982;Ingebrigtsen et al, 1985). Although very little is known about reproductive toxicity of paraquat in humans, at least two separate incidences of paraquat poisoning of pregnant women have been reported in the literature: one involving an accidental exposure *Present address: Drug Safety Evaluations, McNeil Pharmaceutical, Spring House, PA 19477, U.S.A. tTo whom reprint requests should be addressed.…”

Section: Introductionmentioning

confidence: 99%

Human placental lipid peroxidation—II. NADPH and iron dependent stimulation of microsomal lipid peroxidation by paraquat

Kenel

Bestervelt

Kulkarni

1987

General Pharmacology: The Vascular System

View full text Add to dashboard Cite

Paraquat, a widely used herbicide, was found to cause a marked stimulation of lipid peroxidation in the human placental microsomes in vitro. Both NADPH and chelated iron were necessary to observe paraquat-stimulated lipid peroxidation. The malondialdehyde accumulation in the incubation medium increased with increase in time, protein and paraquat concentration. The reaction did not exhibit the initial lag phase suggesting that endogenous membrane-bound antioxidants in human placental microsomes are either absent or present in extremely small quantities.

show abstract

Distribution and transplacental transfer of paraquat in rats and guinea-pigs

Cited by 16 publications

References 6 publications

A Fetal Risk Factor for Parkinson’s Disease

A Fetal Risk Factor for Parkinson’s Disease

Fetal poisoning after maternal paraquat ingestion during third trimester of pregnancy: Case report and literature review

Human placental lipid peroxidation—II. NADPH and iron dependent stimulation of microsomal lipid peroxidation by paraquat

Contact Info

Product

Resources

About