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pfos和pfosa分别通过pparγ和ahr通路引起斑马鱼胚胎心脏畸形
首发时间：2024-06-28
摘要：全氟辛烷磺酸（pfos）及其前体物全氟辛烷磺酰胺（pfosa）在环境中广泛存在。研究表明，孕妇暴露于pfos/pfosa与后代先天性心脏病之间存在强烈关联，但具体机制尚不明确。我们假设pfos和pfosa通过过氧化物酶体增殖物激活受体γ（pparγ）和芳香烃受体（ahr）途径分别引起心脏缺陷。在本研究中，我们证明了将斑马鱼胚胎暴露于pfosa或pfos会引起心脏畸形和功能障碍。pfos和pfosa均能引起斑马鱼胚胎心脏中活性氧（ros）的过量产生、线粒体损伤和细胞凋亡。通过抑制剂阻断pparγ仅能减轻pfos引起的变化，而不能影响pfosa。相反，抑制ahr能减轻pfosa引起的不良影响，但对pfos无效。总之，我们的研究表明，pfos和pfosa通过pparγ和ahr途径分别引起过量的ros产生，这种氧化应激导致线粒体损伤和细胞凋亡，最终引起心脏缺陷。
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pfos and pfosa induce cardiac defects in zebrafish via pparγ and ahr pathways
abstract：perfluorooctane sulfonate (pfos) and its precursor, perfluorooctane sulfonamide (pfosa), are widespread in the environment. evidence suggests a strong link between maternal exposure to pfos/pfosa and congenital heart diseases in offspring, but the mechanisms remain unclear. we hypothesized that pfos and pfosa induce cardiac defects through the peroxisome proliferator-activated receptor gamma (pparγ) and aryl hydrocarbon receptor (ahr) pathways, respectively. in this study, we demonstrated that exposing zebrafish embryos to either pfosa or pfos caused cardiac malformations and dysfunction. both pfos and pfosa induced reactive oxygen speciespfos and pfosa induce cardiac defects in zebrafish via pparγ and ahr pathways (ros) overproduction, mitochondrial damage, and apoptosis in zepfos and pfosa induce cardiac defects in zebrafish via pparγ and ahr pathways, respectively#brafish embryonic hearts. blockade of pparγ through pharmaceutical inhibitor or genetic knockdown only attenuated the changes caused by pfos, not by pfosa. conversely, inhibition of ahr alleviated the adverse effects induced by pfosa but not by pfos. in summary, our findings indicate that pfos and pfosa induce excessive ros production via the pparγ and ahr pathways, respectively. this oxidative stress leads to mitochondrial damage and apoptosis, resulting in cardiac defects.?????
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pfos和pfosa分别通过pparγ和ahr通路引起斑马鱼胚胎心脏畸形
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