Imlay James A
Department of Microbiology, University of Illinois, Urbana, Illinois 61801, USA.
Annu Rev Microbiol. 2003;57:395-418. doi: 10.1146/annurev.micro.57.030502.090938.
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.
氧中毒现象普遍存在，但直到最近我们才开始从分子层面理解其原理。氧化还原酶具有众所周知的非特异性，会将电子传递给与之发生电子接触的任何良好受体。这给需氧生物带来了一个问题，因为分子氧足够小，能够穿透除了氧化还原酶最隐蔽的活性位点之外的所有位点。偶然的电子传递给氧会产生超氧化物和过氧化氢，它们是部分还原的物种，能够氧化那些氧本身难以与之反应的生物分子。本综述试图阐述我们对细胞内活性氧如何形成以及它们损伤特定靶分子的机制仍不完整的理解。细胞对氧化的易感性是专性厌氧、自发诱变以及将氧化应激用作生物武器的根源。
