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首页> 外文期刊>Radiation Research: Official Organ of the Radiation Research Society >RADIATION-INDUCED CELL LETHALITY OF SALMONELLA TYPHIMURIUM ATCC 14028 - COOPERATIVE EFFECT OF HYDROXYL RADICAL AND OXYGEN
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RADIATION-INDUCED CELL LETHALITY OF SALMONELLA TYPHIMURIUM ATCC 14028 - COOPERATIVE EFFECT OF HYDROXYL RADICAL AND OXYGEN

机译：辐射性鼠伤寒沙门氏菌ATCC 14028的细胞亲和力-羟基自由基和氧气的协同作用

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The lethality of gamma-radiation doses of 0.2 to 1.0 kGy for Salmonella typhimurium ATCC 14028 was measured in the presence of air, N-2 and N2O and with the hydroxyl radical scavengers formate and polyethylene glycol (PEG), M(r) 8,000. Saturation of cell suspensions with either N2O or N-2/N2O (1:1, v/v) gas was expected to double the number of hydroxyl radicals (OH.) and to produce an equivalent increase in lethality, but this did not occur. Adding 10% (v/v) O-2 to either N-2 or N2O gas produced approximately the same gamma-irradiation lethality for S. typhimurium as did air. Addition of hydroxyl radical scavengers, 40 mill formate and 1.5% (w/v) PEG, significantly reduced the lethality of gamma radiation for S. typhimurium in the presence of air but not in the presence of N-2 or N2O gases. Membrane-permeable formate provided slightly better protection than nonpermeable PEG. Cells of S. typhimurium grown under anaerobic conditions were more sensitive to radiation, and were less protected by hydroxyl radical scavengers, especially formate, than when cells grown under aerobic conditions were irradiated in the presence of oxygen. Hydroxyl radical scavengers provided no further protection during irradiation in the absence of oxygen. These results indicated that the increased radiation sensitivity of cells grown under anaerobic conditions may be related to superoxide radicals which could increase intercellular damage during irradiation in the presence of oxygen. However, endogenous superoxide dismutase and catalase activities did not protect cells from the radiation-induced lethality of S. typhimurium. Cytoplasmic extracts protected bacterial DNA in vitro in either the presence or absence of oxygen, and no radiation-induced lipid peroxidation of the cellular components was identified by measuring the levels of 2-thiobarbituric acid. These results suggest that most radiation-induced cell lethality was related to the cooperative effects of extracellular OH. and O-2 on the cell surface as the radiation dose increased. (C) 1995 by Radiation Research Society [References: 38]
机译：在空气，N-2和N2O以及羟基自由基清除剂甲酸酯和聚乙二醇（PEG），M（r）8,000的存在下，测定了鼠伤寒沙门氏菌ATCC 14028的0.2至1.0 kGyγ辐射致死率。用N2O或N-2 / N2O（1：1，v / v）气体使细胞悬液饱和可望使羟基自由基（OH。）的数量增加一倍，并导致杀伤力的增加，但这种情况并未发生。向N-2或N2O气体中添加10％（v / v）O-2对鼠伤寒沙门氏菌产生的γ辐射致死率与空气大致相同。在空气存在下，但在N-2或N2O气体存在下，添加羟基自由基清除剂，40毫升甲酸盐和1.5％（w / v）PEG，显着降低了鼠伤寒沙门氏菌的伽马辐射致死性。膜可渗透的甲酸酯提供的保护性比不可渗透的PEG略好。与在氧气条件下在有氧条件下生长的细胞相比，在厌氧条件下生长的鼠伤寒沙门氏菌细胞对辐射更敏感，并且受到羟基自由基清除剂（尤其是甲酸盐）的保护较少。羟基自由基清除剂在无氧辐射期间没有提供进一步的保护。这些结果表明，在厌氧条件下生长的细胞对辐射的敏感性增加可能与超氧自由基有关，而超氧自由基可能会在有氧条件下的辐射过程中增加细胞间的损伤。但是，内源性超氧化物歧化酶和过氧化氢酶活性不能保护细胞免受辐射引起的鼠伤寒沙门氏菌的致死性。细胞质提取物在有氧或无氧条件下均可在体外保护细菌DNA，并且通过测量2-硫代巴比妥酸的水平未鉴定出辐射诱导的细胞成分脂质过氧化。这些结果表明大多数辐射诱导的细胞致死率与细胞外OH的协同作用有关。随着辐射剂量的增加，细胞表面的O-2和O-2含量增加。 （C）1995年，辐射研究学会[参考文献：38]

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