Oxidative stress during development: Chemical-induced teratogenesis
Oxidative stress during development: Chemical-induced teratogenesis
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DOI：
10.1016/j.cotox.2017.11.003
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发表时间：
2018-02-01
影响因子：
4.6
通讯作者：
Piorczynski, Ted B.
中科院分区：
文献类型：
--
作者：
Hansen, Jason M.;Jacob, Benjamin R.;Piorczynski, Ted B.
氧化应激已被证明是导致出生缺陷的重要因素，包括结构畸形和神经行为缺陷。在高水平，氧化应激促进细胞凋亡，但在不会导致细胞死亡的低水平，氧化还原敏感的通路可能会被破坏。导致出生缺陷的化学品通常会提供非常不同的发育结果，这取决于妊娠期间的暴露时间和暴露水平，但这些观察也表明，特定缺陷的表现涉及特定的途径。在这里，我们回顾了氧化应激及其在发育过程中的影响的主要主题，并提供了一些最臭名昭著的人类致畸物质的具体例子，这些致畸物质产生氧化应激作为其致畸机制的一部分。展望未来，未来的研究应该集中在对发育过程中氧化还原敏感因素的更深刻理解，以开发潜在的预防性干预措施。
Oxidative stress has been shown to be an important contributor to birth defects, including structural malformation and neurobehavioral deficits. At high levels, oxidative stress promotes apoptosis but at lower levels that do not cause cell death, redox-sensitive pathways can be disrupted. Chemicals that cause birth defects usually provide a very distinct developmental outcome, dependent upon gestational periods of exposure and level of exposure, but these observations also suggest that there are specific pathways involved in the manifestation of a given defect. Here, we review overarching themes of oxidative stress and their effects during development and provide specific examples of some of the most notorious human teratogens that produce oxidative stress as part of their teratogenic mechanism. Moving forward, future studies should center on providing a more profound understanding of redox-sensitive elements during development to develop potential preventative interventions.