发育期PFOS暴露的肺损伤效应及机制研究
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摘要
目的:由于宫内PFOS暴露导致的子代死亡风险增加可能与PFOS的肺毒性相关,因此本研究旨在探讨胚胎期PFOS暴露致仔鼠肺损伤及可能的毒性机制。
方法:将雌、雄性成熟SD大鼠按2:1合笼后,经阴道涂片筛选受孕的雌鼠。然后将孕鼠随机分为对照组(0.05% Tween-20)、低剂量组(0.1 mg/kg/day PFOS)、高剂量组(2 mg/kg/day PFOS)。从母鼠受孕后第2天(gestational day 1,GD1)开始进行PFOS灌胃染毒,直至分娩结束。染毒体积为1 ml/kg。对出生后的仔鼠观察其3日内存活率及初生至断奶期间的体重增长情况。同时将初生(PND 0)和断奶期(PND 21)仔鼠经麻醉后处死,收集血液、肺脏等主要脏器。采用液相色谱-质谱串联(LC/MS/MS)分析血清及肺脏组织中PFOS的浓度,用H&E染色法、TUNEL技术、Real-time PCR、western blotting、酶学技术等分别检测肺脏的病理学改变、肺部细胞凋亡、细胞凋亡调控分子mRNA表达水平、cyt c蛋白的释放、caspase 3、8、9的酶活力,同时还检测了肺脏中MDA水平、GSH的含量以及SOD酶的活力等氧化损伤相关指标。
结果:与对照组和低剂量组相比,孕鼠妊娠期高剂量PFOS暴露能明显诱导PND 0和PND 21仔鼠肺脏肺泡出血、肺间隔增厚、炎性浸润、肺实变等病理学改变,TUNEL显示高剂量组仔鼠肺组织出现明显的细胞凋亡(P<0.01)。胚胎期高剂量PFOS暴露组仔鼠肺脏Bax、Fas以及FasL的mRNA表达在PND 0和21明显上调(P<0.01),Bcl-2 mRNA水平在PND 0显著下调(P<0.01),而且胞浆cyt c蛋白的释放水平在PND 0和PND 21均明显增加(P<0.01),caspase 3、8、9酶的活力在PND 0和21也显著提高(P<0.01);此外,高剂量组仔鼠肺脏在PND 0和PND 21 MDA水平明显增加(P<0.01)、还原性生物分子GSH的含量显著减少、抗氧化酶SOD活力下降(P<0.01)。在低剂量组,仔鼠肺组织中没有明显的病理改变和细胞凋亡,3种caspase酶的活力没有明显改变,只是PND 0仔鼠肺脏的bax mRNA表达和MDA水平,以及PND 21肺脏Fas mRNA表达会轻微上调(P<0.05)。结论:宫内PFOS暴露能够引起仔鼠肺组织的损伤,而且这种损伤具有一定的持
续性。本实验证实氧化应激损伤和细胞程序性死亡参与了肺组织的损伤过程,而且内源性和外源性凋亡通路均被活化。
目的:在第一部分的动物研究结果显示,氧化损伤和细胞凋亡在胚胎期PFOS暴露致仔鼠肺损伤中起到了非常重要的作用。但尚不能断定这些损伤效应是PFOS对肺组织的直接毒作用。因此,该部分通过建立体外细胞染毒模型,探讨PFOS对肺上皮细胞株A549的直接毒效应。
方法:通过将A549细胞在1%血清浓度培养基培养条件下,暴露于不同浓度的PFOS(0、12.5、25、50、100、200μM)一定时间后,用MTT法、流式细胞术、DCFH-DA荧光探针、JC-1荧光探针等分别检测细胞活力、细胞凋亡率、胞内ROS的产生以及线粒体膜电位;此外还检测了MDA水平、GSH含量以及SOD酶活力等氧化应激指标;用酶学的方法还检测了caspase 3、caspase 8、caspase 9三种酶的活力。此外,还探讨了用还原剂NAC预处理后,通过检测ROS的产生、细胞活力和凋亡率,看ROS是否介导了PFOS的毒效应。最后,还初步研究了不同血清浓度下(1%和10%)PFOS的毒性差异。
结果:与溶剂对照组相比,A549细胞在低血清环境下(1%)经不同浓度的PFOS处理24-72 h后,细胞活力呈剂量和时间依赖性下降。此外,在该血清浓度下暴露于PFOS,细胞凋亡率、ROS的产生、MDA水平、SOD酶活力、caspase 3和caspase 9的活力呈剂量依赖性增加,同时,胞内GSH含量和线粒体膜电位均下降。但各暴露组细胞胞内caspase 8的活力并没有上升,甚至在低剂量组还有轻度下降。NAC预处理能显著抑制PFOS诱导的ROS的产生、细胞活力下降以及细胞凋亡。另外,在10%血清浓度培养条件下暴露于PFOS,只有最高剂量组(200μM)细胞出现活力下降,而且高血清能显著抑制200μM PFOS造成的细胞凋亡。
结论:PFOS通过ROS介导的内源性细胞凋亡通路诱导A549细胞凋亡。同时高血清培养条件能够抑制PFOS的细胞毒性,可能与血清蛋白结合PFOS有关,或许这可以用来解释发育期PFOS暴露比成年期暴露更敏感的原因。
Objective: The main purpose of this study was to investigate the ability of prenatal PFOS exposure to induce oxidation and apoptosis in rat offspring lungs.
Methods: Pregnant rats were dosed orally with PFOS (0, 0.1 and 2.0 mg/kg/day) from gestation days (GD) 1 to 21. Lung samples from postnatal day (PND) 0 and 21 pups were analyzed for the toxic effects of PFOS. The content of PFOS in serum and lung was analyzed using LC/MS/MS, H&E staining, TUNEL, Real time PCR and western blot were used to detect the histopathological changes, cell apoptosis, the expression of proapoptotic and antiapoptotic molecules mRNA, respectively. In addition, the release of cytochrome c (Cyt c) from mitochondria to cytoplasm, the activities of caspase 3, 8, 9 and SOD, levels of MDA, GSH were also detected. Results: The concentrations of PFOS in sera and lung were also increased in a
dose-dependent manner. Compared to the controls, significant differences in body weight from PND 0 to PND 21and postnatal mortality within PND 3 were observed in the high dose group. It was shown that dams that received 2.0 mg/kg/day caused sever histopathological changes along with marked oxidative injuries and increased cell apoptosis in neonatal lungs, and further examinations showed that the ratio of Bax to Bcl-2, release of cyt c from mitochondria, expressions of proapoptotic genes (Fas and Fas-L), and activities of caspase-3, -8 and -9 were up-regulated correspondingly. There was no significant histopathological change and cell apoptosis in neonatal lungs at the low dose group, even though the level of MDA and bax mRNA of PND 0 lungs, and the expression of Fas mRNA of PND 21 lungs, were increased slightly.
Conclution: In summary, the present study demonstrated that prenatal PFOS exposure could overwhelm the homeostasis of antioxidative systems to result in oxidative stress and activate both caspase-dependent death pathways in rat offspring lungs.
Objective: The main purpose of this study was to investigate the direct effects of PFOS on A549 lung epithelial cells, since the study in part 1 could not distinguish whether the pulmonary toxicity induced by prenatal PFOS exposure represented direct lung toxic mechanisms as any of the innumerable possibilities from cryptic and overt systemic toxicity.
Methods: After A549 cells were exposed to various concentration of PFOS (0-200μM),MTT, flow cytometry, DCFH-DA, and JC-1 were used to detect cell viability, cell apoptosis rate, ROS level and mitochondrial membrane potential (MMP), respectively. Levels of MDA and GSH, activities of SOD, caspase 3, 8, and 9 were also evaluated. In addition, we further investigated the protective effects of NAC against PFOS-induced cell apoptosis, and the different responses of A549 to PFOS under cultures supplemented with different concentration sera.
Results: Compared to controls, after 24 h, 48 h or 72 h of PFOS exposure, the cell viabilities were clearly decreased in concentration and time-dependent manners. Furthermore, cell apoptosis rate, levels of ROS, MDA, activities of SOD, caspase 3 and 9, were increased, while levels of GSH and MMP were inclined significantly, after 24 h of PFOS exposure. Pre-treatment with NAC for 2 h obviously suppressed PFOS-induced increase of intracellular ROS levels, cell viability loss and apoptosis. In addition, it was also found that the addition of sera protected the cells from the detrimental effects of PFOS.
Conclusion: PFOS has the obvious toxic effects on A549 cells, and the intrinsic cell death pathway, activated by ROS-mediated mitochondrial dysfunction, takes part in the PFOS-induced A549 cell apoptosis. In light of the protective effect of sera, the fact that the fetus and newborn possess lower content of these proteins suggested that greater lung toxicity may occur at blood levels of PFOS that are nontoxic to adults. Keywords:PFOS, A549, apoptosis, ROS, mitochondrial injury
方法:将雌、雄性成熟SD大鼠按2:1合笼后,经阴道涂片筛选受孕的雌鼠。然后将孕鼠随机分为对照组(0.05% Tween-20)、低剂量组(0.1 mg/kg/day PFOS)、高剂量组(2 mg/kg/day PFOS)。从母鼠受孕后第2天(gestational day 1,GD1)开始进行PFOS灌胃染毒,直至分娩结束。染毒体积为1 ml/kg。对出生后的仔鼠观察其3日内存活率及初生至断奶期间的体重增长情况。同时将初生(PND 0)和断奶期(PND 21)仔鼠经麻醉后处死,收集血液、肺脏等主要脏器。采用液相色谱-质谱串联(LC/MS/MS)分析血清及肺脏组织中PFOS的浓度,用H&E染色法、TUNEL技术、Real-time PCR、western blotting、酶学技术等分别检测肺脏的病理学改变、肺部细胞凋亡、细胞凋亡调控分子mRNA表达水平、cyt c蛋白的释放、caspase 3、8、9的酶活力,同时还检测了肺脏中MDA水平、GSH的含量以及SOD酶的活力等氧化损伤相关指标。
结果:与对照组和低剂量组相比,孕鼠妊娠期高剂量PFOS暴露能明显诱导PND 0和PND 21仔鼠肺脏肺泡出血、肺间隔增厚、炎性浸润、肺实变等病理学改变,TUNEL显示高剂量组仔鼠肺组织出现明显的细胞凋亡(P<0.01)。胚胎期高剂量PFOS暴露组仔鼠肺脏Bax、Fas以及FasL的mRNA表达在PND 0和21明显上调(P<0.01),Bcl-2 mRNA水平在PND 0显著下调(P<0.01),而且胞浆cyt c蛋白的释放水平在PND 0和PND 21均明显增加(P<0.01),caspase 3、8、9酶的活力在PND 0和21也显著提高(P<0.01);此外,高剂量组仔鼠肺脏在PND 0和PND 21 MDA水平明显增加(P<0.01)、还原性生物分子GSH的含量显著减少、抗氧化酶SOD活力下降(P<0.01)。在低剂量组,仔鼠肺组织中没有明显的病理改变和细胞凋亡,3种caspase酶的活力没有明显改变,只是PND 0仔鼠肺脏的bax mRNA表达和MDA水平,以及PND 21肺脏Fas mRNA表达会轻微上调(P<0.05)。结论:宫内PFOS暴露能够引起仔鼠肺组织的损伤,而且这种损伤具有一定的持
续性。本实验证实氧化应激损伤和细胞程序性死亡参与了肺组织的损伤过程,而且内源性和外源性凋亡通路均被活化。
目的:在第一部分的动物研究结果显示,氧化损伤和细胞凋亡在胚胎期PFOS暴露致仔鼠肺损伤中起到了非常重要的作用。但尚不能断定这些损伤效应是PFOS对肺组织的直接毒作用。因此,该部分通过建立体外细胞染毒模型,探讨PFOS对肺上皮细胞株A549的直接毒效应。
方法:通过将A549细胞在1%血清浓度培养基培养条件下,暴露于不同浓度的PFOS(0、12.5、25、50、100、200μM)一定时间后,用MTT法、流式细胞术、DCFH-DA荧光探针、JC-1荧光探针等分别检测细胞活力、细胞凋亡率、胞内ROS的产生以及线粒体膜电位;此外还检测了MDA水平、GSH含量以及SOD酶活力等氧化应激指标;用酶学的方法还检测了caspase 3、caspase 8、caspase 9三种酶的活力。此外,还探讨了用还原剂NAC预处理后,通过检测ROS的产生、细胞活力和凋亡率,看ROS是否介导了PFOS的毒效应。最后,还初步研究了不同血清浓度下(1%和10%)PFOS的毒性差异。
结果:与溶剂对照组相比,A549细胞在低血清环境下(1%)经不同浓度的PFOS处理24-72 h后,细胞活力呈剂量和时间依赖性下降。此外,在该血清浓度下暴露于PFOS,细胞凋亡率、ROS的产生、MDA水平、SOD酶活力、caspase 3和caspase 9的活力呈剂量依赖性增加,同时,胞内GSH含量和线粒体膜电位均下降。但各暴露组细胞胞内caspase 8的活力并没有上升,甚至在低剂量组还有轻度下降。NAC预处理能显著抑制PFOS诱导的ROS的产生、细胞活力下降以及细胞凋亡。另外,在10%血清浓度培养条件下暴露于PFOS,只有最高剂量组(200μM)细胞出现活力下降,而且高血清能显著抑制200μM PFOS造成的细胞凋亡。
结论:PFOS通过ROS介导的内源性细胞凋亡通路诱导A549细胞凋亡。同时高血清培养条件能够抑制PFOS的细胞毒性,可能与血清蛋白结合PFOS有关,或许这可以用来解释发育期PFOS暴露比成年期暴露更敏感的原因。
Objective: The main purpose of this study was to investigate the ability of prenatal PFOS exposure to induce oxidation and apoptosis in rat offspring lungs.
Methods: Pregnant rats were dosed orally with PFOS (0, 0.1 and 2.0 mg/kg/day) from gestation days (GD) 1 to 21. Lung samples from postnatal day (PND) 0 and 21 pups were analyzed for the toxic effects of PFOS. The content of PFOS in serum and lung was analyzed using LC/MS/MS, H&E staining, TUNEL, Real time PCR and western blot were used to detect the histopathological changes, cell apoptosis, the expression of proapoptotic and antiapoptotic molecules mRNA, respectively. In addition, the release of cytochrome c (Cyt c) from mitochondria to cytoplasm, the activities of caspase 3, 8, 9 and SOD, levels of MDA, GSH were also detected. Results: The concentrations of PFOS in sera and lung were also increased in a
dose-dependent manner. Compared to the controls, significant differences in body weight from PND 0 to PND 21and postnatal mortality within PND 3 were observed in the high dose group. It was shown that dams that received 2.0 mg/kg/day caused sever histopathological changes along with marked oxidative injuries and increased cell apoptosis in neonatal lungs, and further examinations showed that the ratio of Bax to Bcl-2, release of cyt c from mitochondria, expressions of proapoptotic genes (Fas and Fas-L), and activities of caspase-3, -8 and -9 were up-regulated correspondingly. There was no significant histopathological change and cell apoptosis in neonatal lungs at the low dose group, even though the level of MDA and bax mRNA of PND 0 lungs, and the expression of Fas mRNA of PND 21 lungs, were increased slightly.
Conclution: In summary, the present study demonstrated that prenatal PFOS exposure could overwhelm the homeostasis of antioxidative systems to result in oxidative stress and activate both caspase-dependent death pathways in rat offspring lungs.
Objective: The main purpose of this study was to investigate the direct effects of PFOS on A549 lung epithelial cells, since the study in part 1 could not distinguish whether the pulmonary toxicity induced by prenatal PFOS exposure represented direct lung toxic mechanisms as any of the innumerable possibilities from cryptic and overt systemic toxicity.
Methods: After A549 cells were exposed to various concentration of PFOS (0-200μM),MTT, flow cytometry, DCFH-DA, and JC-1 were used to detect cell viability, cell apoptosis rate, ROS level and mitochondrial membrane potential (MMP), respectively. Levels of MDA and GSH, activities of SOD, caspase 3, 8, and 9 were also evaluated. In addition, we further investigated the protective effects of NAC against PFOS-induced cell apoptosis, and the different responses of A549 to PFOS under cultures supplemented with different concentration sera.
Results: Compared to controls, after 24 h, 48 h or 72 h of PFOS exposure, the cell viabilities were clearly decreased in concentration and time-dependent manners. Furthermore, cell apoptosis rate, levels of ROS, MDA, activities of SOD, caspase 3 and 9, were increased, while levels of GSH and MMP were inclined significantly, after 24 h of PFOS exposure. Pre-treatment with NAC for 2 h obviously suppressed PFOS-induced increase of intracellular ROS levels, cell viability loss and apoptosis. In addition, it was also found that the addition of sera protected the cells from the detrimental effects of PFOS.
Conclusion: PFOS has the obvious toxic effects on A549 cells, and the intrinsic cell death pathway, activated by ROS-mediated mitochondrial dysfunction, takes part in the PFOS-induced A549 cell apoptosis. In light of the protective effect of sera, the fact that the fetus and newborn possess lower content of these proteins suggested that greater lung toxicity may occur at blood levels of PFOS that are nontoxic to adults. Keywords:PFOS, A549, apoptosis, ROS, mitochondrial injury
引文
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