title: Trichloroethylene exposure aggravates behavioral abnormalities in mice that are deficient in superoxide dismutase.
abstract: Trichloroethylene (TCE) has been implicated as a causative agent for Parkinson's disease (PD). The administration of TCE to rodents induces neurotoxicity associated with dopaminergic neuron death, and evidence suggests that oxidative stress as a major player in the progression of PD. Here we report on TCE-induced behavioral abnormality in mice that are deficient in superoxide dismutase 1 (SOD1). Wild-type (WT) and SOD1-deficient (Sod1(-/-)) mice were intraperitoneally administered TCE (500 mg/kg) over a period of 4 weeks. Although the TCE-administrated Sod1(-/-) mice showed marked abnormal motor behavior, no significant differences were observed among the experimental groups by biochemical and histopathological analyses. However, treating mouse neuroblastoma-derived NB2a cells with TCE resulted in the down regulation of the SOD1 protein and elevated oxidative stress under conditions where SOD1 production was suppressed. Taken together, these data indicate that SOD1 plays a pivotal role in protecting motor neuron function against TCE toxicity.
authors.affiliation: Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Otsuki
authors.affiliation: Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
authors.forename: Takujiro
authors.initials: T
authors.lastname: Homma
authors.affiliation: Department of Physiology, Yamagata University School of Medicine, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
authors.forename: Hiroki
authors.initials: H
authors.lastname: Fujiwara
authors.affiliation: Department of Physiology, Yamagata University School of Medicine, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
authors.forename: Kenya
authors.initials: K
authors.lastname: Kaneko
authors.affiliation: Department of Anatomy and Cell Biology, Yamagata University School of Medicine, Iidanishi 2-2-2, Yamagata 990-9585, Japan.
authors.forename: Yasukazu
authors.initials: Y
authors.lastname: Hozumi
authors.affiliation: Health Research Institute (HRI), National Institute of Advanced Industrial Science and Technology (AIST), 1-8-31 Midorigaoka, Ikeda, Osaka 563-8577, Japan.
authors.forename: Mototada
authors.initials: M
authors.lastname: Shichiri
authors.affiliation: Health Research Institute (HRI), National Institute of Advanced Industrial Science and Technology (AIST), 1-8-31 Midorigaoka, Ikeda, Osaka 563-8577, Japan.
authors.forename: Mizuki
authors.initials: M
authors.lastname: Takashima
authors.affiliation: Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
authors.forename: Junitsu
authors.initials: J
authors.lastname: Ito
authors.affiliation: Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
authors.forename: Tasuku
authors.initials: T
authors.lastname: Konno
authors.affiliation: Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Kurahashi
authors.affiliation: Health Research Institute (HRI), National Institute of Advanced Industrial Science and Technology (AIST), 2217-14 Hayashi-cho, Takamatsu, Kagawa 761-0395, Japan.
authors.forename: Yasukazu
authors.initials: Y
authors.lastname: Yoshida
authors.affiliation: Department of Anatomy and Cell Biology, Yamagata University School of Medicine, Iidanishi 2-2-2, Yamagata 990-9585, Japan.
authors.forename: Kaoru
authors.initials: K
authors.lastname: Goto
authors.affiliation: Department of Physiology, Yamagata University School of Medicine, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Fujii
authors.affiliation: Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata 990-9585, Japan. Electronic address: jfujii@med.id.yamagata-u.ac.jp.
authors.forename: Junichi
authors.initials: J
authors.lastname: Fujii
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D001921:Brain / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D045744:Cell Line, Tumor; D059290:Dopaminergic Neurons / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D005838:Genotype; D018345:Mice, Knockout; D009043:Motor Activity / Q000187:drug effects*; D009447:Neuroblastoma / Q000201:enzymology / Q000473:pathology; D020258:Neurotoxicity Syndromes / Q000201:enzymology / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D018384:Oxidative Stress / Q000187:drug effects; D010641:Phenotype; D045442:Rotarod Performance Test; D000072105:Superoxide Dismutase-1 / Q000172:deficiency* / Q000235:genetics; D013997:Time Factors; D014241:Trichloroethylene / Q000633:toxicity*
chemical_list: D014241:Trichloroethylene; C000606291:Sod1 protein, mouse; D000072105:Superoxide Dismutase-1
keywords: Neurotoxicity; Oxidative stress; Parkinson’s disease; Superoxide dismutase; Trichloroethylene