The phenomenon of oxygen toxicity is universal, but only recently have we begun to understand its basis in molecular terms. Redox enzymes are notoriously nonspecific, transferring electrons to any good acceptor with which they make electronic contact. This poses a problem for aerobic organisms, since molecular oxygen is small enough to penetrate all but the most shielded active sites of redox enzymes. Adventitious electron transfers to oxygen create superoxide and hydrogen peroxide, which are partially reduced species that can oxidize biomolecules with which oxygen itself reacts poorly. This review attempts to present our still-incomplete understanding of how reactive oxygen species are formed inside cells and the mechanisms by which they damage specific target molecules. The vulnerability of cells to oxidation lies at the root of obligate anaerobiosis, spontaneous mutagenesis, and the use of oxidative stress as a biological weapon.

中文翻译：

---

氧化损伤的途径。

氧中毒现象是普遍现象，但直到最近，我们才开始从分子角度了解其基础。众所周知，氧化还原酶是非特异性的，可以将电子转移到与其进行电子接触的任何良好受体上。这对有氧生物来说是个问题，因为分子氧足够小，足以穿透除氧化还原酶以外最受保护的活性位点。偶然的电子转移到氧气上会产生超氧化物和过氧化氢，它们是部分还原的物种，可以氧化生物分子，而氧气本身与之反应不良。这篇综述试图提出我们关于细胞内活性氧如何形成以及它们如何破坏特定靶分子的机制的不完全理解。