title: Arsenic-induced inhibition of hippocampal neurogenesis and its reversibility.
abstract: Arsenic exposure can result in damages of the neurological system. The present study aimed at whether cell proliferation and neurogenesis in the adult mouse hippocampus were affected after arsenic exposure and whether they could recover after exposure cessation. Mice were randomly placed into 3 groups. The first group received distilled water alone for 4 months (control group); the second group received 4.0 mg/L As(2)O(3) through drinking water for 4 months (arsenic group); the third group received 4.0 mg/L As(2)O(3) for 2 months and then changed to distilled water for another 2 months (recovery group). Serum and cerebrum arsenic concentrations of the arsenic group were significantly elevated, and then decreased to normal after the change of arsenic to water in the diet. After a four-month administration, the hippocampal number of proliferative cells and the percentage of new mature neurons decreased in the arsenic group as compared with the control group, however, increased significantly in the recovery group when compared with the arsenic group, and restored to the control level. There were no significant differences for apoptosis in different groups. Obvious histopathological ameliorations were observed in the hippocampus of the recovery group. The inhibition of hippocampus cell proliferation and neurogenesis by arsenic is reversible after the arsenic administration was terminated.
authors.affiliation: Department of Occupational and Environmental Health, Dalian Medical University, Dalian 116044, PR China.
authors.forename: Shuang
authors.initials: S
authors.lastname: Liu
authors.forename: Fengyuan
authors.initials: F
authors.lastname: Piao
authors.forename: Xiance
authors.initials: X
authors.lastname: Sun
authors.forename: Lulu
authors.initials: L
authors.lastname: Bai
authors.forename: Yan
authors.initials: Y
authors.lastname: Peng
authors.forename: Yuanxia
authors.initials: Y
authors.lastname: Zhong
authors.forename: Ning
authors.initials: N
authors.lastname: Ma
authors.forename: Wenchang
authors.initials: W
authors.lastname: Sun
mesh_terms: D000818:Animals; D001151:Arsenic / Q000378:metabolism / Q000633:toxicity*; D001973:Bromodeoxyuridine / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D020287:In Situ Nick-End Labeling; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009433:Neural Inhibition / Q000187:drug effects*; D055495:Neurogenesis / Q000187:drug effects*; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D020127:Recovery of Function / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D060508:Wnt3 Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D060508:Wnt3 Protein; D010751:Phosphopyruvate Hydratase; D001973:Bromodeoxyuridine; D001151:Arsenic