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Effects of Ultraviolet Radiation on Respiration and Growth in Radiation-resistant and Radiation-sensitive Strains of Escherichia coli B

机译:紫外线辐射对大肠杆菌B抗辐射和辐射敏感菌株呼吸和生长的影响

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Ultraviolet (UV) irradiation at 254 nm causes different respiration and growth responses in log-phase cultures of Escherichia coli B/r and Bs?1. These differences are correlated with the ability and inability, respectively, of these bacterial strains to repair UV-induced lesions in deoxyribonucleic acid (DNA). After irradiation, Bs?1 cells (radiation-sensitive) exhibit uncoupling of growth and respiration; growth and synthesis cease, whereas respiration continues. B/r cells (radiation-resistant) grown on glycerol exhibit severe temporary inhibition of growth and respiration after UV, and the coupling of these two processes is maintained, except at a very high UV dose. Inhibition begins at about the time DNA synthesis resumes and continues for a period of time that is dependent upon dose. Glucose-grown cells do not exhibit severe respiratory, growth, and synthetic inhibitions; these processes remain coupled in the cells during the postirradiation period. Photoreactivation treatment delays uncoupling of growth and respiration in Bs?1 and prevents inhibition of respiration and growth in B/r. These results indicate that the postirradiation responses result from the presence of pyrimidine dimers in DNA. Ultraviolet irradiation of B/r and Bs?1 cells results in an accumulation of adenosine triphosphate by 30 min after UV. This accumulation decreases with time and does not appear to be related to the inhibition of respiration in glycerol-grown B/r cells. The results on B/r are interpreted in terms of a control mechanism for reestablishment of a balance among macromolecules in the irradiated cells so as to provide them with the potential to survive. The specific steps in such a reestablishment of balance appear to depend upon the substrate oxidized. In Bs?1 cells, which cannot repair UV-induced damage in DNA, some control mechanism that coordinates cellular processes may be inactivated.
机译:254 nm的紫外线(UV)引起大肠杆菌 B / r和B s?1 的对数期培养产生不同的呼吸和生长反应。这些差异分别与这些细菌菌株修复脱氧核糖核酸(DNA)中紫外线诱导的损伤的能力和无能力相关。辐射后,B s?1 细胞(辐射敏感)表现出生长和呼吸的解偶联;生长和合成停止,而呼吸继续。在甘油上生长的B / r细胞(抗辐射)在UV后表现出对生长和呼吸的严重暂时抑制,并且除了非常高的UV剂量外,这两个过程的耦合得以维持。抑制作用大约在DNA合成恢复时开始,并持续一段时间,具体取决于剂量。葡萄糖生长的细胞不表现出严重的呼吸,生长和合成抑制作用。这些过程在辐照后期间保持耦合在细胞中。光活化处理延迟了B s?1 中生长和呼吸的解偶联,并阻止了B / r对呼吸和生长的抑制。这些结果表明辐照后反应是由于DNA中存在嘧啶二聚体引起的。 B / r和B s?1 细胞的紫外线照射导致紫外线照射30分钟后三磷酸腺苷蓄积。这种积累随时间减少,似乎与甘油生长的B / r细胞中的呼吸抑制无关。关于B / r的结果是根据用于重建被照射细胞中的大分子之间的平衡的控制机制来解释的,从而为它们提供了生存的潜力。这种重新建立平衡的具体步骤似乎取决于被氧化的底物。在不能修复UV诱导的DNA损伤的B s?1 细胞中,一些协调细胞过程的控制机制可能会失活。

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