Formaldehyde induces the bone marrow toxicity in mice by regulating the expression of Prx3 protein.
10.1007/s11596-015-1393-6
- Author:
Guang-yan YU
1
;
Xiang-fu SONG
;
Shu-hua ZHAO
;
Ying LIU
;
Zhi-wei SUN
Author Information
1. Department of Preventative Medicine, School of Public Health, Jilin University, Changchun, 130021, China, yugy@jlu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Blotting, Western;
Bone Marrow;
drug effects;
metabolism;
Formaldehyde;
pharmacology;
Homeodomain Proteins;
metabolism;
Male;
Mice
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2015;35(1):82-86
- CountryChina
- Language:English
-
Abstract:
Formaldehyde (FA) is a ubiquitous toxic organic compound, and it has been regarded as a leukemogen. However, the mechanisms by which FA induces bone marrow toxicity remain unclear. The present study was aimed to examine the bone marrow toxicity caused by FA and the mechanism involving the expression changes of peroxiredoxin3 (Prx3) in this process. The mice were divided into four groups with 6 mice per group. Animals in the control group were exposed to ambient air and those in the FA groups to different concentrations of FA (20, 40, 80 mg/m(3)) for 15 days in the separate inhalation chambers, 2 h a day. At the end of the 15-day experimental period, all mice were killed. Bone marrow cells were obtained. The level of hydrogen peroxide (H2O2), the apoptosis rate, and the activities and protein expression levels of caspase-3 and caspase-9 were determined by biochemical assay, flow cytometry and immunohistochemistry, respectively; DNA damage and Prx3 expression levels were measured by single cell gel eletrophoresis immunohistochemistry and Western blotting, respectively. The results showed that the H2O2 level and cell apoptosis rate were significantly increased in FA groups relative to the control group. Caspase-3 and caspase-9 activities and their protein expression levels were markedly increased as well. Additionally, FA also increased the rate of DNA damage and the expression level of Prx3 compared with control group. Our study suggested that a certain concentration of FA causes the bone marrow toxicity by regulating the expression of Prx3.
