Contrary to frequent reports in the literature, hydroxyl radical is not a key species participating in endogenous oxidative DNA damage. Instead, carbonate radical anion is formed from the Fenton reaction under cellular conditions and from decomposition of nitrosoperoxycarbonate generated during inflammation. Carbonate radical anion is a potent one-electron oxidant capable of generating base radical cations that can migrate over long distances in duplex DNA, ultimately generating 8-oxo-7,8-dihydroguanine at a redox-sensitive sequence such as GGG. Such a mechanism enables G-quadruplex-forming sequences to act as long-range sensors of oxidative stress, impacting gene expression via the DNA repair mechanism that reads and ultimately erases the oxidized base. With a writing, reading and erasing mechanism in place, oxidative ‘damage’ to DNA might be relabeled as ‘epigenetic’ modifications.

中文翻译：

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羟基自由基与氧化应激引起的 DNA 损伤的无关性及其对表观遗传学的影响。

与文献中经常报道的相反，羟自由基并不是参与内源性DNA氧化损伤的关键物种。相反，碳酸根阴离子是由细胞条件下的芬顿反应和炎症过程中产生的亚硝基过氧碳酸盐的分解形成的。碳酸根阴离子是一种有效的单电子氧化剂，能够产生碱基自由基阳离子，这些阳离子可以在双链体 DNA 中长距离迁移，最终在氧化还原敏感序列（如 GGG）处生成 8-oxo-7,8-二氢鸟嘌呤。这种机制使 G-四链体形成序列能够充当氧化应激的远程传感器，通过读取并最终擦除氧化碱基的 DNA 修复机制影响基因表达。有了写入、读取和擦除机制，DNA 的氧化“损伤”可能会被重新标记为“表观遗传”修饰。