Zeng Huai-Cai, He Qing-Zhi, Li Yuan-Yuan, Wu Cheng-Qiu, Wu Yi-Mou, Xu Shun-Qing
Post-Doctoral Mobile Stations for Basic Medicine, University of South China, Hengyang, 421001, People's Republic of China.
Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Environ Toxicol. 2015 Sep;30(9):1082-90. doi: 10.1002/tox.21981. Epub 2014 Mar 11.
Perfluorooctanyl sulfonate (PFOS), a cardiac toxicity compound, has been widely detected in the environment and in organisms. However, the toxic mechanism is not clear. Our previous study indicated that prenatal PFOS exposure led to swollen mitochondrial with vacuolar structure and loss of cristae in offsping's heart. The purpose of this study was to investigate the effect of PFOS on the apoptosis in developing heart and mitochondria-mediated apoptosis pathway. Pregnant Sprague-Dawley (SD) rats were exposed to PFOS at doses of 0.1, 0.6, and 2.0 mg/kg-d and 0.05% Tween 80 as control by gavage from gestation day 2 (GD 2) to GD 21. Apoptosis, as well as expression of apoptosis related genes associated with mitochondrial-mediated apoptosis pathway, including p53, bcl-2, bax, cytochrome c, caspase-9, and caspase-3 were analyzed in heart tissues from weaned (postnatal day 21, PND 21) offspring. The results showed that prenatal PFOS exposure resulted in apoptosis in the offspring's heart. The mRNA and protein expression levels of p53, bax, cytochrome c, caspase-9, and caspase-3 in the offspring's heart were enhanced in various PFOS-treated groups, meanwhile, the bcl-2 expression levels were decreased. Our results indicated that prenatal PFOS exposure induced the apoptosis of weaned offspring rat heart tissue via mitochondria-mediated apoptotic pathway.
全氟辛烷磺酸（PFOS）是一种具有心脏毒性的化合物，已在环境和生物体中被广泛检测到。然而，其毒性机制尚不清楚。我们之前的研究表明，产前暴露于PFOS会导致子代心脏线粒体肿胀，出现空泡结构，嵴消失。本研究的目的是探讨PFOS对发育中心脏细胞凋亡及线粒体介导的凋亡途径的影响。将怀孕的Sprague-Dawley（SD）大鼠从妊娠第2天（GD 2）至GD 21通过灌胃给予0.1、0.6和2.0 mg/kg-d的PFOS，以0.05%吐温80作为对照。分析断奶（出生后第21天，PND 21）子代心脏组织中的细胞凋亡情况，以及与线粒体介导的凋亡途径相关的凋亡相关基因的表达，包括p53、bcl-2、bax、细胞色素c、caspase-9和caspase-3。结果表明，产前暴露于PFOS会导致子代心脏细胞凋亡。在各个PFOS处理组中，子代心脏中p53、bax、细胞色素c、caspase-9和caspase-3的mRNA和蛋白表达水平均升高，同时，bcl-2表达水平降低。我们的结果表明，产前暴露于PFOS通过线粒体介导的凋亡途径诱导断奶子代大鼠心脏组织细胞凋亡。
