摘要:
十溴联苯醚(decabromodiphenyl ether,BDE-209)是目前应用最广泛的的溴系阻燃剂,其环境风险引起很大关注。本实验以小鼠肾脏和脑组织为实验材料,研究了离体条件下BDE-209的急性氧化损伤效应。BDE-209染毒终浓度设置为0,1,2,4和8 μg·mL-1,采用NBT和TBA法分别测定SOD (superoxide dismutase)活性和MDA (malondialdehyde)含量。结果显示,随着BDE-209染毒浓度的升高,小鼠肾脏和脑组织的SOD活性先升高后降低,较高染毒浓度组的SOD活性与对照组相比显著性降低;MDA含量逐渐上升,并且与对照组相比较高染毒浓度组的MDA含量显著上升。以上结果说明,离体条件下BDE-209对小鼠肾脏和脑组织能够产生急性氧化应激,并导致脂质过氧化损伤。
Abstract:
As a most widely used brominated flame retardant, potential environmental risk of decabromodiphenyl ether (BDE-209) has been attracted more and more attention. In this experiment, the acute oxidative damage effect of BDE-209 on mouse kidney and brain tissues was performed. Mouse kidney and brain cells were exposed to different doses (0, 1, 2, 4, 8 μ g·mL-1) of BDE-209 in vitro, and enzymatic activity of superoxide dismutase (SOD) content of malondialdehyde (MDA) were determined. Our results showed that SOD activity in mouse kidney and brain tissue were activated at low doses and inhibited at high doses. In highest dose group, SOD activity was even lower than that of the control group. MDA content in kidney and brain cells gradually increased as BDE-209 concentration increased, which was significantly higher in the experimental groups than that in the control group. These results indicated that BDE-209 could induce acute oxidative stress on mouse kidney and brain tissue in vitro, resulting in lipid peroxidation damage.
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