Science：两项研究证实抗生素的杀伤作用与活性氧簇(ROS)生成无关
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近年来，微生物学领域涌现出的一系列研究均表明，抗生素借助了一种普遍的杀伤机制：以相同的途径促使细菌细胞生成了称作活性氧簇（ROS）的化合物。
然而，近日，东北大学（Northeastern University）和伊利诺伊大学（University of Illinois）的两项独立研究反驳了上面提及的“一刀切”的选择性假设。他们发现，抗生素的杀伤作用与ROS生成无关。相关研究发表在近期出版的《科学》（Science）杂志上。
研究发现，即使细菌无法生成ROS，仍易受到抗生素影响。此外，一些抗生素在需氧和厌氧两种条件下均能挥舞他们的“致命魔术棒”，而活性氧簇只能在有氧条件下才会形成。
研究小组在有氧和缺氧两种情况下用抗生素处理了细菌培养物。为了的变量是气体环境，其他处理完全相同。研究人员发现两个种群之间的细胞死亡没有差异。
在开展这些实验之前，研究人员首先检测了一种荧光染料的信号，这种荧光染料通常被科学家用作ROS水平指示剂。研究人员用各种抗生素处理了细菌细胞，并检测了这一信号的强度。由于假定抗生素会提高ROS水平，研究人员预计抗生素浓度增高会与强信号相关。然而，他们却没有看到这样的相关性。
为了用明确的数据支持他们的观察结果，研究小组成员将具有较强荧光信号的细胞从弱信号的细胞分离出来，用相同的抗生素处理它们。结果，两个群体经受了相等的细胞死亡。
研究表明，与当前的观点相反，抗生素显然没有通过诱导活性氧簇来杀伤细菌。研究结果相当清楚，但也给研究人员留下了一个谜题——抗菌药物到底是如何帮助感染人群清除细菌感染的？
有了这些研究结果，研究人员希望该研究领域能够将焦点放到在了解抗生素消灭细菌的真实机制上，以有效解决慢性细菌感染，这才是当今公共健康面临的最紧迫问题。
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Killing by Bactericidal Antibiotics Does Not Depend on Reactive Oxygen Species
Science 8 March 2013 | DOI: 10.1126/science.1232688
Bactericidal antibiotics kill by modulating their respective targets. This traditional view has been challenged by studies that propose an alternative, unified mechanism of killing, whereby toxic reactive oxygen species (ROS) are produced in the presence of antibiotics. We found no correlation between an individual cell's probability of survival in the presence of antibiotic and its level of ROS. An ROS quencher, thiourea, protected cells from antibiotics present at low concentrations, but the effect was observed under anaerobic conditions as well. There was essentially no difference in survival of bacteria treated with various antibiotics under aerobic or anaerobic conditions. This suggests that ROS do not play a role in killing of bacterial pathogens by antibiotics.
Cell Death from Antibiotics Without the Involvement of Reactive Oxygen Species
Science 8 March 2013 | DOI: 10.1126/science.1232751
Recent observations have suggested that classic antibiotics kill bacteria by stimulating the formation of reactive oxygen species (ROS). If true, this notion might guide new strategies to improve antibiotic efficacy. In this study, the model was directly tested. Contrary to the hypothesis, antibiotic treatment did not accelerate the formation of hydrogen peroxide in Escherichia coli and did not elevate intracellular free iron, an essential reactant for the production of lethal damage. Lethality persisted in the absence of oxygen, and DNA repair mutants were not hypersensitive, undermining the idea that toxicity arose from oxidative DNA lesions. We conclude that these antibiotic exposures did not produce ROS and that lethality more likely resulted from the direct inhibition of cell-wall assembly, protein synthesis, and DNA replication.
