title: Prenatal exposure to permethrin influences vascular development of fetal brain and adult behavior in mice offspring.
abstract: Pyrethroids are one of the most widely used classes of insecticides and show neurotoxic effects that induce oxidative stress in the neonatal rat brain. However, little is still known about effects of prenatal exposure to permethrin on vascular development in fetal brain, central nervous system development, and adult offspring behaviors. In this study, the effects of prenatal exposure to permethrin on the development of cerebral arteries in fetal brains, neurotransmitter in neonatal brains, and locomotor activities in offspring mice were investigated. Permethrin (0, 2, 10, 50, and 75 mg/kg) was orally administered to pregnant females once on gestation day 10.5. The brains of permethrin-treated fetuses showed altered vascular formation involving shortened lengths of vessels, an increased number of small branches, and, in some cases, insufficient fusion of the anterior communicating arteries in the area of circle of Willis. The prenatal exposure to permethrin altered neocortical and hippocampus thickness in the mid brain and significantly increased norepinephrine and dopamine levels at postnatal day 7 mice. For spontaneous behavior, the standing ability test using a viewing jar and open-field tests showed significant decrease of the standing ability and locomotor activity in male mice at 8 or 12 weeks of age, respectively. The results suggest that prenatal exposure to permethrin may affect insufficient development of the brain through alterations of vascular development.
authors.affiliation: Health Risk Research Section, Center for Environmental Risk Research, National Institute for Environmental Studies 16-2, Onogawa, Tsukuba, Ibaraki 305-8506, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Imanishi
authors.forename: Masahiro
authors.initials: M
authors.lastname: Okura
authors.forename: Hiroko
authors.initials: H
authors.lastname: Zaha
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Hiromi
authors.initials: H
authors.lastname: Akanuma
authors.forename: Reiko
authors.initials: R
authors.lastname: Nagano
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Shiraishi
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Fujimaki
authors.forename: Hideko
authors.initials: H
authors.lastname: Sone
mesh_terms: D020533:Angiogenesis Inhibitors / Q000633:toxicity; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000098:blood supply / Q000187:drug effects* / Q000196:embryology / Q000254:growth & development; D002536:Cerebral Arteries / Q000002:abnormalities; D004298:Dopamine / Q000378:metabolism; D005260:Female; D005333:Fetus; D007306:Insecticides / Q000633:toxicity*; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects; D051379:Mice; D008813:Mice, Inbred ICR; D009043:Motor Activity; D018919:Neovascularization, Physiologic / Q000187:drug effects; D018377:Neurotransmitter Agents / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D018384:Oxidative Stress; D026023:Permethrin / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology / Q000523:psychology*; D051381:Rats; D013792:Thalidomide / Q000633:toxicity
chemical_list: D020533:Angiogenesis Inhibitors; D007306:Insecticides; D018377:Neurotransmitter Agents; D013792:Thalidomide; D026023:Permethrin; D004298:Dopamine; D009638:Norepinephrine
keywords: cerebral arteries; fetal exposure; mice; pyrethroids