Department of Biochemistry and Molecular Biology, College of Medicine, Howard University, 520 W Street, NW, Washington, DC 20059, USA.
Department of Biochemistry, Faculty of Applied Medical Science, Umm Al- Qura University, Makkah 21421, Saudi Arabia.
Int J Mol Sci. 2019 Jan 16;20(2):364. doi: 10.3390/ijms20020364.
Oxidative stress and the resulting damage to DNA are inevitable consequence of endogenous physiological processes further amplified by cellular responses to environmental exposures. If left unrepaired, oxidative DNA lesions can block essential processes such as transcription and replication or can induce mutations. Emerging data also indicate that oxidative base modifications such as 8-oxoG in gene promoters may serve as epigenetic marks, and/or provide a platform for coordination of the initial steps of DNA repair and the assembly of the transcriptional machinery to launch adequate gene expression alterations. Here, we briefly review the current understanding of oxidative lesions in genome stability maintenance and regulation of basal and inducible transcription.
氧化应激以及由此导致的 DNA 损伤是内源性生理过程的必然结果，而细胞对环境暴露的反应进一步放大了这一过程。如果这些损伤得不到修复，氧化 DNA 损伤可能会阻断转录和复制等基本过程，或导致基因突变。新出现的数据还表明，氧化碱基修饰，如基因启动子中的 8-氧鸟嘌呤，可能作为表观遗传标记，和/或为 DNA 修复的初始步骤以及转录机制的组装提供一个平台，以启动适当的基因表达改变。在这里，我们简要回顾了目前对氧化损伤在基因组稳定性维持以及基础转录和诱导转录调控中的作用的理解。
