全氟辛烷磺酰基化合物对剑尾鱼肝脏抗氧化物酶活性的影响

Effects of perfluorooctane sulfonate on hepatic antioxidant enzyme activities in swordtails (Xiphophorus helleri)

目的研究全氟辛烷磺酰基化合物(PFOS)暴露对剑尾鱼(Xiphophorus helleri Heckel)抗氧化物酶活性的影响,探讨PFOS对鱼类的致毒机理。方法使用浸润法以3.5、7.0、14.0和28.0 mg/L四个PFOS浓度为剑尾鱼染毒,定量测定了96 h内肝脏组织中的超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)活性及丙二醛(MDA)含量的变化。结果 PFOS暴露12 h后,除28.0 mg/L组SOD活性被显著性抑制外,其余各组与对照组均无显著性差异(P>0.05);7.0 mg/L组和14.0 mg/L组在24 h被极显著诱导(P<0.01),并且一直保持至96 h。CAT活性随PFOS浓度的升高而降低,12 h时,除3.5 mg/L组外,其余各组CAT活性被显著或极显著抑制,至24 h时,各组CAT活性有上升趋势,但48 h后,各组呈不断下降趋势持续至96 h,其CAT活性恢复到12 h水平。GSH-PX活性变化与CAT活性变化趋势相似,其中28.0 mg/L组在不同时间均被显著性抑制,并在96 h时抑制率达到最高值64.8%。MDA含量在12 h时呈小幅下降趋势,但随着暴露时间的延长,各处理组MDA含量呈连续上升趋势,并在96 h时达到最高点,诱导率分别为71.2%、70.1%和85.1%。结论结果表明,SOD的高活性是由于机体中超氧阴离子的存在,而高浓度的超氧阴离子能够灭活CAT和GSH-PX活性,因此,CAT和GSH-PX活性始终低于对照组。GSH-PX对PFOS的敏感性高于CAT。MDA含量持续升高反映出细胞组织已经遭受到氧化损伤。剑尾鱼活体的实验表明,PFOS能够诱导肝脏氧化应激反应,氧化损伤是PFOS致毒的主要途径之一。

Objective To study the effect of acute perfluorooctane sulfonate （PFOS） exposure on induction of ox- idative stress in the liver of swordtails （Xiphophorus heller~ Heckel） in order to explore the toxic mechanism of PFOS in fish. Methods Swordtails were randomly divided into five groups, with one control group and four experimental groups （3.5 mg/L, 7.0 rag/L, 14. 0 mg/L, and 28.0 mg/L PFOS） , 20 fish in each group. Parallel experimental groups were al- so established. The oxidative stress index （malondialdehyde aldehyde, MDA ） and activities of superoxide dismutase （ SOD）, catalase （CAT） , and glutathione peroxidase （GSH-PX） in the fish livers were determined after 12 h, 24 h, 48 h, and 96 h exposure. Results After 12 h exposure to PFOS, the 28.0 mg/L exposure group exhibited significant inhibi-tion of SOD activity. However, in comparison with the control group, there were no significant differences in the other three groups （P 〉0. 05）. SOD activity was significantly induced in two exposure groups （7.0 mg/L and 14.0 mg/L） after 24 h exposure and this upward trend was maintained to 96 h. SOD activity increased during the early hours of exposure and reached a maximal value at 24 h, at which point there was a significant difference with that of the control group, before de- creasing gradually and eventually resuming an upward trend at 96 h. This pattern suggests that such activity may be related to PFOS in the biological body through the elimination mechanism of enterohepatic circulation. Over the same time frame, CAT activity decreased as the concentration of PFOS increased. Three groups （7.0 mg/L, 14.0 mg./L, and 28.0 mg/L） were significantly inhibited at 12 h. CAT activity in each group exhibited slight upward trend, but remained lower than the level observed in the control group after 24 h exposure. After 48 h, each group showed a decreasing trend that continued until 96 h and their CAT activity returned to the level recorded at 12 h. Although the changing trends in GSH-PX and CAT activity were observed to be similar, GSH-PX activity in the 28 mg./L exposure group exhibited significant inhibition at each time point. MDA content decreased slightly at 12 h exposure, indicating the influence of bio-metabolic changes or other physiological factors rather than oxidative stress was involved. However, as the exposure time prolonged, the MDA content of each group continued to increase and reached a maximal value at 96 h. Conclusions The results of this study show that a relative high concentration of PFOS has an apparent effect on antioxidant enzyme activities in swordtail livers. The results of swordtail in vivo experiments therefore show that PFOS can induce oxidative stress in the liver and that PFOS-induced ox- idative damage is a major route for this toxic effect.