title: Formaldehyde induces bone marrow toxicity in mice by inhibiting peroxiredoxin 2 expression.
abstract: Peroxiredoxin 2 (Prx2), a member of the peroxiredoxin family, regulates numerous cellular processes through intracellular oxidative signal transduction pathways. Formaldehyde (FA)-induced toxic damage involves reactive oxygen species (ROS) that trigger subsequent toxic effects and inflammatory responses. The present study aimed to investigate the role of Prx2 in the development of bone marrow toxicity caused by FA and the mechanism underlying FA toxicity. According to the results of the preliminary investigations, the mice were divided into four groups (n=6 per group). One group was exposed to ambient air and the other three groups were exposed to different concentrations of FA (20, 40, 80 mg/m3) for 15 days in the respective inhalation chambers, for 2 h a day. At the end of the 15-day experimental period, all of the mice were sacrificed and bone marrow cells were obtained. Cell samples were used for the determination of pathology, glutathione peroxidase (GSH-Px) activity and myeloperoxidase (MPO) activity and protein expression; as well as for the determination of DNA damage and Prx2 expression. The results revealed an evident pathological change in the FA-treated groups, as compared with the controls. In the FA treatment group GSH-Px activity was decreased, while MPO activity and protein expression were increased. The rate of micronucleus and DNA damage in the FA-treated groups was also increased and was significantly different compared with the control, while the expression of Prx2 was decreased. The present study suggested that at certain concentrations, FA had a toxic effect on bone marrow cells and that changes in the Prx2 expression are involved in this process.
authors.affiliation: Department of Preventative Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
authors.forename: Guangyan
authors.initials: G
authors.lastname: Yu
authors.affiliation: Department of Preventative Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Chen
authors.affiliation: Department of Preventative Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Hygenic Toxicology, School of Public Health, Capital Medical University, Beijing 100069, P.R. China.
authors.forename: Caixia
authors.initials: C
authors.lastname: Guo
authors.affiliation: Department of Preventative Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
authors.forename: Haiying
authors.initials: H
authors.lastname: Du
authors.affiliation: Department of Preventative Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
authors.forename: Zhiwei
authors.initials: Z
authors.lastname: Sun
mesh_terms: D000818:Animals; D001853:Bone Marrow / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004249:DNA Damage / Q000187:drug effects*; D005557:Formaldehyde / Q000633:toxicity*; D005979:Glutathione Peroxidase / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009195:Peroxidase / Q000378:metabolism; D054464:Peroxiredoxins / Q000378:metabolism*
chemical_list: D005557:Formaldehyde; D054464:Peroxiredoxins; D009195:Peroxidase; D005979:Glutathione Peroxidase