Effect of chromate stress on Escherichia coli K-12
Effect of chromate stress on Escherichia coli K-12
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DOI：
10.1128/jb.188.9.3371-3381.2006
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发表时间：
2006-05-01
影响因子：
3.2
通讯作者：
Matin, A
中科院分区：
文献类型：
--
作者：
Ackerley, DF;Barak, Y;Matin, A
研究了暴露于铬酸盐的大肠杆菌K-12所经历的应力的性质，以及可能使细胞能够承受这种应力的机制。在铬酸盐存在下通过过夜生长预适应的细胞比未适应的对照组应力更小。在3它的铬酸盐暴露，后者停止生长，并表现出极端的丝状形态; 5它有部分恢复与相对正常的细胞形态的恢复。相比之下，预适应细胞的形态和生长受到的影响较小。细胞的氧化应激，通过使用的H2 O2-响应的荧光染料监测，是最严重的非适应细胞在接种后3小时，较低的部分恢复的细胞在接种后5小时，和更低的预适应的细胞。铬酸盐暴露耗尽细胞水平的还原型谷胱甘肽和其他游离巯基在更大程度上比预适应的细胞在非适应。在这两种细胞类型中，SOS反应被激活，并且可以对抗氧化应激的蛋白质如SodB和CysK的水平增加。一些缺失抗氧化蛋白的突变体（SodB、CysK、YieF或KatE）对铬酸盐更敏感。因此，氧化应激在体内铬酸盐毒性中起主要作用，并且针对这种毒性的细胞防御涉及抗氧化机制的激活。由于细菌铬酸盐生物修复受到铬酸盐毒性的限制，因此在细菌铬酸盐还原过程中最大限度地减少氧化应激并增强这些生物应对这种应激的能力将提高其在铬酸盐生物修复中的有效性。
The nature of the stress experienced by Escherichia coli K-12 exposed to chromate, and mechanisms that may enable cells to withstand this stress, were examined. Cells that had been preadapted by overnight growth in the presence of chromate were less stressed than nonadapted controls. Within 3 It of chromate exposure, the latter ceased growth and exhibited extreme filamentous morphology; by 5 It there was partial recovery with restoration of relatively normal cell morphology. In contrast, preadapted cells were less drastically affected in their morphology and growth. Cellular oxidative stress, as monitored by use of an H2O2-responsive fluorescent dye, was most severe in the nonadapted cells at 3 h postinoculation, lower in the partially recovered cells at 5 h postinoculation, and lower still in the preadapted cells. Chromate exposure depleted cellular levels of reduced glutathione and other free thiols to a greater extent in nonadapted than preadapted cells. In both cell types, the SOS response was activated, and levels of proteins such as SodB and CysK, which can counter oxidative stress, were increased. Some mutants missing antioxidant proteins (SodB, CysK, YieF, or KatE) were more sensitive to chromate. Thus, oxidative stress plays a major role in chromate toxicity in vivo, and cellular defense against this toxicity involves activation of antioxidant mechanisms. As bacterial chromate bioremediation is limited by the toxicity of chromate, minimizing oxidative stress during bacterial chromate reduction and bolstering the capacity of these organisms to deal with this stress will improve their effectiveness in chromate bioremediation.