Gene mutation and micronucleus assays in gpt delta mice treated with 2,2′,4,4′- tetrabromodiphenyl ether

被引:5
|
作者
You, Xinyue [1 ,2 ]
Ando, Tomoko [3 ]
Xi, Jing [1 ,2 ]
Cao, Yiyi [1 ,2 ]
Liu, Weiying [1 ,2 ]
Zhang, Xinyu [1 ,2 ]
Honma, Masamitsu [3 ]
Masumura, Kenichi [3 ]
Luan, Yang [1 ,2 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Hongqiao Int Inst Med, Shanghai Tong Ren Hosp, Shanghai 200025, Peoples R China
[2] Shanghai Jiao Tong Univ, Fac Publ Hlth, Sch Med, Shanghai 200025, Peoples R China
[3] Natl Inst Hlth Sci, Div Genet & Mutagenesis, Setagaya Ku, 1-18-1 Kamiyoga, Tokyo 1588501, Japan
基金
中国国家自然科学基金;
关键词
POLYBROMINATED DIPHENYL ETHERS; PIG-A; FLAME RETARDANTS; CANCER CELLS; DNA-DAMAGE; BDE-47; GENOTOXICITY; TOXICITY; EXPOSURE; CYTOTOXICITY;
D O I
10.1093/mutage/gey002
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Flame retardant polybrominated diphenyl ethers (PBDEs) are a class of persistent organic pollutants (POPs). 2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) is a representative PBDE congener with widespread distribution and relatively high toxicity potential. Although it has been reported that BDE-47 can cause DNA damage in various in vitro systems, few studies have provided in vivo genotoxicity information. The aim of the present study was to investigate the genotoxicity of BDE-47 in mice. Male gpt delta mice were administered BDE-47 by gavage at 0, 0.0015, 1.5, 10 and 30 mg/kg/day, and 6 days per week for six consecutive weeks. Before the first treatment, and at 2.5 and 5 weeks after the first treatment, peripheral blood was collected from tails and the micronucleus assay and the Pig-a gene mutation assay were performed. After the last treatment, the mutant frequencies of the gpt gene in the liver and the germ cells from seminiferous tubules were determined. All these assays failed to produce positive results, suggesting that BDE-47 was neither clastogenic nor mutagenic in both target and non-target tissues in gpt delta mice.
引用
收藏
页码:153 / 160
页数:8
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