PURE SINGLET OXYGEN CYTOTOXICITY FOR BACTERIA
PURE SINGLET OXYGEN CYTOTOXICITY FOR BACTERIA
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DOI：
10.1111/j.1751-1097.1987.tb04779.x
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发表时间：
1987-09-01
影响因子：
3.3
通讯作者：
HARTMAN, PE
中科院分区：
文献类型：
--
作者：
DAHL, TA;MIDDEN, WR;HARTMAN, PE
我们已经修改了先前描述的分离表面敏化剂单线态氧产生系统（Midden和Wang，1983），用于有效暴露于膜过滤器上收集的细菌的纯单线态氧。光敏剂和细菌的物理分离消除了细菌和光激发的敏化剂之间直接相互作用的可能性，所述直接相互作用可能导致I型（非单线态氧）光氧化过程。该系统被用于检测单线态氧的细菌细胞毒性。通过测量随着单线态氧源和细菌之间的距离增加细胞毒性的降低来证实单线态氧的作用。负责细胞杀伤的中间体的气相半衰期由该距离依赖性分析确定（24 . ±. 6 ms），与由文献数据计算的单线态氧的气相半衰期相同（53 ± 0.6ms）。37 ms）。在相同剂量的单线态氧下，比较了对各种鼠伤寒沙门氏菌和大肠杆菌菌株的杀灭作用。细菌被杀死的单线态氧在几个数量级低于那些有效杀死H2 O2。改变DNA修复能力（uvrB，recA，xth，nth，pKM 101）不影响生存。单线态氧暴露后，不完全的细胞壁脂多糖形成降低了存活率。单线态氧猝灭剂组氨酸的过量产生增加了存活，二肽肌肽（β-肌肽）的积累也是如此。丙氨酰-L-组氨酸）。在各种沙门氏菌中未获得外源单线态氧暴露的致突变性证据。鼠伤寒菌株被杀死至35%的存活率。
We have modified the separated-surface-sensitizer singlet oxygen generating system previously described (Midden and Wang, 1983) for the efficient exposure to pure singlet oxygen of bacteria collected on membrane filters. Physical separation of the photosensitizer and the bacteria eliminates the possibility of direct interaction between bacteria and photoexcited sensitizers that could lead to Type I (non-singlet oxygen) photooxidation processes. This system was used to examine the bacterial cytotoxicity of singlet oxygen. The role of singlet oxygen was confirmed by measuring the decrease in cytotoxicity as the distance between the singlet oxygen source and the bacteria was increased. The gas phase half-life of the intermediate responsible for cell killing, determined from this distance dependence analysis (24 .+-. 6 ms), is the same as that calculated from literature data for the gas phase half-life of singlet oxygen (53 .+-. 37 ms). Killing of various strains of Salmonella typhimurium and Escherichia coli was compared at the same dose of singlet oxygen. Bacteria were killed by singlet oxygen at levels several orders of magnitude lower than those effective in killing by H2O2. Altered DNA repair capacities (uvrB, recA, xth, nth, pKM101) did not affect survival. Incomplete cell wall lipopolysaccharide formation decreased survival following singlet oxygen exposure. Overproduction of the singlet oxygen quencher histidine increased survival, as did accumulation of the dipeptide carnosine (.beta.-alanyl-L-histidine). No evidence for mutagenicity of exogenous singlet oxygen exposure was obtained in a variety of S. typhimurium strains killed to 35% survival.