GENERAL MECHANISM FOR THE BACTERIAL TOXICITY OF HYPOCHLOROUS ACID - ABOLITION OF ATP PRODUCTION
GENERAL MECHANISM FOR THE BACTERIAL TOXICITY OF HYPOCHLOROUS ACID - ABOLITION OF ATP PRODUCTION
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DOI：
10.1021/bi00449a032
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发表时间：
1989-11-14
期刊：
影响因子：
2.9
通讯作者：
HURST, JK
中科院分区：
文献类型：
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作者：
BARRETTE, WC;HANNUM, DM;HURST, JK
腺苷酸能荷（EC）的大肠杆菌25922，铜绿假单胞菌27853，和乳酸链球菌7962迅速下降，在营养丰富的媒体从超过0.9的值低于0.1时，生物体暴露于致命水平的HOCl。维持在能量耗尽状态的相同细胞在HOCl暴露后用营养能量源挑战时不能达到生物合成和生长所必需的正常EC值。这些变化与复制能力的丧失定量相关。葡萄糖、琥珀酸和作为呼吸底物的各种氨基酸的初始转运速率以及E.大肠杆菌25922也在活力丧失的同时或之前下降。这些结果证实，细胞死亡伴随着细菌ATP生产的完全破坏，通过氧化和发酵途径，作为抑制内膜结合系统负责这些过程的结果。
The adenylate energy charges (EC) of Escherichia coli 25922, Pseudomonas aeruginosa 27853, and Streptococcus lactis 7962 rapidly fell in nutrient-rich media from values in excess of 0.9 to below 0.1 when the organisms were exposed to lethal levels of HOCl. The same cells maintained in energy-depleted states were incapable of attaining normal EC values necessary for biosynthesis and growth when challenged with nutrient energy sources after HOCl exposure. These changes correlated quantitatively with loss of replicative capabilities. Initial rates of transport of glucose, succinate, and various amino acids that act as respiratory substrates and the ATP hydrolase activity of the F1 complex from the ATP synthase of E. coli 25922 also declined in parallel with or preceded loss of viability. These results establish that cellular death is accompanied by complete disruption of bacterial ATP production by both oxidative and fermentative pathways as a consequence of inhibition of inner membrane bound systems responsible for these processes.