Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai, PR China.
J Environ Sci Health A Tox Hazard Subst Environ Eng. 2011;46(12):1320-7. doi: 10.1080/10934529.2011.602937.
In the present study, the cytotoxic effects and toxicological mechanism of six polybrominated diphenyl ethers (PBDEs) metabolites (3-OH-BDE47, 3-MeO-BDE47, 5-OH-BDE47, 5-MeO-BDE47, 6-OH-BDE85 and 6-MeO-BDE85) on L02 cells were explored by investigating the cell viability, apoptosis, lactic dehydrogenase (LDH) leakage, and oxidative stress response. The results showed that these metabolites could inhibit cell proliferation and induce apoptosis, among which 6-OH-BDE85 had the highest efficiency. LDH leakage test also showed that 6-OH-BDE85 had the strongest ability to cause LDH release. The reactive oxygen species (ROS) levels in 6-OH-BDE85- and 3-OH-BDE47-treated groups were significantly elevated in a dose-dependent manner. After treatment for 24 h, four BDE47 metabolites (3-OH-BDE47, 3-MeO-BDE47, 5-OH-BDE47, and 5-MeO-BDE47) induced an increase in superoxide dismutase (SOD) activity and decrease in glutathione (GSH) level, whereas 6-OH-BDE85 led to a decrease in both SOD activity and GSH level. These effects disappeared after continued culturing for another 24 h. In conclusion, these PBDE metabolites, especially 6-OH-BDE85, showed cytotoxicity on L02 cells, which was at least partially related to the oxidative stress level.
在本研究中，通过研究细胞活力、细胞凋亡、乳酸脱氢酶（LDH）渗漏和氧化应激反应，探讨了六种多溴二苯醚（PBDE）代谢物（3-OH-BDE47、3-MeO-BDE47、5-OH-BDE47、5-MeO-BDE47、6-OH-BDE85 和 6-MeO-BDE85）对 L02 细胞的细胞毒性作用和毒理学机制。结果表明，这些代谢物可以抑制细胞增殖并诱导细胞凋亡，其中 6-OH-BDE85 效率最高。LDH 渗漏试验也表明 6-OH-BDE85 具有最强的引起 LDH 释放的能力。6-OH-BDE85 和 3-OH-BDE47 处理组的活性氧（ROS）水平呈剂量依赖性显著升高。处理 24 h 后，四种 BDE47 代谢物（3-OH-BDE47、3-MeO-BDE47、5-OH-BDE47 和 5-MeO-BDE47）诱导超氧化物歧化酶（SOD）活性增加和谷胱甘肽（GSH）水平降低，而 6-OH-BDE85 导致 SOD 活性和 GSH 水平均降低。继续培养 24 h 后，这些影响消失。总之，这些 PBDE 代谢物，特别是 6-OH-BDE85，对 L02 细胞表现出细胞毒性，至少部分与氧化应激水平有关。
