Hexabromocyclododecane-induced Genotoxicity in Cultured Human Breast Cells through DNA Damage.

Author: Rui Jing LI ¹ ; Hui GAO ¹ ; Guang Shui NA ¹ ; Zi Hao LU ¹ ; Yao YAO ² ; Fan YANG ¹
Author Information

1. Key Laboratory for Ecological Environment in Coastal Areas, National Marine Environmental Monitoring Center, Dalian 116023, Liaoning, China.
2. Shanghai Ocean University, Shanghai 201306, China.
Publication Type:Letter
MeSH: Breast Neoplasms; chemically induced; genetics; Cell Line, Tumor; DNA Damage; Dose-Response Relationship, Drug; Environmental Pollutants; toxicity; Female; Flame Retardants; toxicity; Humans; Hydrocarbons, Brominated; toxicity; Oxidative Stress; Random Allocation
From: Biomedical and Environmental Sciences 2017;30(4):296-300
CountryChina
Language:English
Abstract: To investigate the genotoxicity and reveal the potential toxicological mechanisms of Hexabromocyclododecane (HBCD), human breast cells HBL-100 were exposed to a sequence of HBCD concentrations (0, 5, 10, and 50 mg/L) for 24 h. With a series of zymology and molecular biology methods, we found that HBCD induced dose-dependent oxidative stress on HBL-100 DNA. As revealed in qRT-PCR, activated prognostic factor ATM down-regulated tumor suppressor gene BRCA1 and prompted DNA repair genes hOGG1 and hMTH1 expression in lower concentrations of HBCD (< 10 mg/L). However, DNA repair were inhibited as well as cell proliferation rate by higher concentrations of HBCD (50 mg/L). The results inferred that the genotoxicity of HBCD was dose-dependent and related to DNA repair pathway.