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首页> 外文期刊>Applied Microbiology >Mechanism of Attenuation of Uranyl Toxicity by Glutathione in Lactococcus lactis
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Mechanism of Attenuation of Uranyl Toxicity by Glutathione in Lactococcus lactis

机译：谷胱甘肽对乳酸乳球菌对尿嘧啶毒性的影响机制

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Both prokaryotic and eukaryotic organisms possess mechanisms for the detoxification of heavy metals, and these mechanisms are found among distantly related species. We investigated the role of intracellular glutathione (GSH), which, in a large number of taxa, plays a role in protection against the toxicity of common heavy metals. Anaerobically grown Lactococcus lactis containing an inducible GSH synthesis pathway was used as a model organism. Its physiological condition allowed study of putative GSH-dependent uranyl detoxification mechanisms without interference from additional reactive oxygen species. By microcalorimetric measurements of metabolic heat during cultivation, it was shown that intracellular GSH attenuates the toxicity of uranium at a concentration in the range of 10 to 150 μM. In this concentration range, no effect was observed with copper, which was used as a reference for redox metal toxicity. At higher copper concentrations, GSH aggravated metal toxicity. Isothermal titration calorimetry revealed the endothermic binding of U(VI) to the carboxyl group(s) of GSH rather than to the reducing thiol group involved in copper interactions. The data indicate that the primary detoxifying mechanism is the intracellular sequestration of carboxyl-coordinated U(VI) into an insoluble complex with GSH. The opposite effects on uranyl and on copper toxicity can be related to the difference in coordination chemistry of the respective metal-GSH complexes, which cause distinct growth phase-specific effects on enzyme-metal interactions.IMPORTANCE Understanding microbial metal resistance is of particular importance for bioremediation, where microorganisms are employed for the removal of heavy metals from the environment. This strategy is increasingly being considered for uranium. However, little is known about the molecular mechanisms of uranyl detoxification. Existing studies of different taxa show little systematics but hint at a role of glutathione (GSH). Previous work could not unequivocally demonstrate a GSH function in decreasing the presumed uranyl-induced oxidative stress, nor could a redox-independent detoxifying action of GSH be identified. Combining metabolic calorimetry with cell number-based assays and genetics analysis enables a novel and general approach to quantify toxicity and relate it to molecular mechanisms. The results show that GSH-expressing microorganisms appear advantageous for uranyl bioremediation.
机译：原核生物和真核生物均具有重金属排毒的机制，并且这些机制在远缘物种中发现。我们研究了细胞内谷胱甘肽（GSH）的作用，该谷胱甘肽在大量生物分类中起着抵抗普通重金属毒性的作用。含有可诱导的GSH合成途径的厌氧生长的乳酸乳球菌被用作模型生物。它的生理条件允许研究假定的GSH依赖性铀酰解毒机理，而不受其他活性氧的干扰。通过微量量热法测量培养期间的代谢热，结果表明，细胞内GSH在10至150μM的浓度范围内会减弱铀的毒性。在该浓度范围内，没有观察到铜的作用，铜被用作氧化还原金属毒性的参考。在较高的铜浓度下，谷胱甘肽会加剧金属毒性。等温滴定量热法显示，U（VI）与GSH的羧基（而不是与铜相互作用涉及的还原巯基）发生吸热结合。数据表明，主要的解毒机理是将羧基配位的U（VI）与GSH结合成不溶性复合物。对铀酰和铜毒性的相反作用可能与各自的金属-谷胱甘肽配合物的配位化学差异有关，后者对酶-金属相互作用产生不同的生长期特异性影响。生物修复，其中微生物用于从环境中去除重金属。越来越多地考虑将这种战略用于铀。但是，关于铀酰解毒的分子机理知之甚少。现有的有关不同分类单元的研究显示很少系统化，但暗示了谷胱甘肽（GSH）的作用。先前的工作不能明确地证明GSH在降低假定的铀酰诱导的氧化应激中的功能，也无法确定GSH的氧化还原依赖性解毒作用。将代谢量热法与基于细胞数的测定法和遗传学分析相结合，可以实现一种新颖且通用的方法来量化毒性并将其与分子机制相关联。结果表明，表达GSH的微生物似乎对铀酰生物修复具有优势。

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