School of Biosciences, University of Birmingham, Birmingham, UK.
FEMS Microbiol Lett. 2011 Dec;325(2):99-107. doi: 10.1111/j.1574-6968.2011.02425.x.
Major questions concerning the sources and mechanisms of the reduction of nitric oxide by enteric bacteria remain unresolved. The membrane-associated nitrate reductase is the major source of NO generated from nitrite, but at least one other source remains to be identified. Nitrite reductases are primarily detoxification systems that decrease rather than increase the accumulation of NO in the cytoplasm. Whether they also catalyze NO formation is unresolved. The FNR protein that regulates transitions between aerobic and anaerobic growth is inactivated as a consequence of nitrosative damage, but we challenge the idea that FNR is a physiologically relevant sensor of NO, except under the most severe nitrosative stress. As none of the three enzymes that reduce NO account for the majority of the rate of NO reduction, additional mechanisms remain to be discovered. Little is known about the biochemistry of damage repair. Whatever the growth conditions and however severe the nitrosative stress, groups of proteins are synthesized to protect the bacterial cytoplasm against the side effects of nitrate and nitrite reduction. The enigmatic hybrid cluster protein is more likely to be part of a repair pathway than a hydroxylamine reductase, as annotated in many genome databases.
关于肠道细菌还原一氧化氮的来源和机制的主要问题仍未解决。膜结合型硝酸盐还原酶是亚硝酸盐生成的一氧化氮的主要来源，但至少还有一个其他来源有待确定。亚硝酸盐还原酶主要是解毒系统，可减少而不是增加细胞质中一氧化氮的积累。它们是否也能催化一氧化氮的形成仍未解决。调节需氧和厌氧生长之间转换的 FNR 蛋白因硝化损伤而失活，但我们质疑 FNR 是一氧化氮生理相关传感器的观点，除非处于最严重的硝化应激状态下。由于没有一种还原一氧化氮的酶可以解释一氧化氮还原的大部分速率，因此仍有待发现其他机制。关于损伤修复的生物化学知之甚少。无论生长条件如何，硝化应激多么严重，都会合成一组蛋白质来保护细菌细胞质免受硝酸盐和亚硝酸盐还原的副作用。正如许多基因组数据库所注释的那样，神秘的杂种簇蛋白更有可能是修复途径的一部分，而不是羟胺还原酶。
