Ramírez-Díaz Martha I, Díaz-Pérez César, Vargas Eréndira, Riveros-Rosas Héctor, Campos-García Jesús, Cervantes Carlos
Instituto de Investigaciones Químico-Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Edificio B-3, Ciudad Universitaria, Morelia, Michoacan 58030, Mexico.
Biometals. 2008 Jun;21(3):321-32. doi: 10.1007/s10534-007-9121-8. Epub 2007 Oct 13.
Chromium is a non-essential and well-known toxic metal for microorganisms and plants. The widespread industrial use of this heavy metal has caused it to be considered as a serious environmental pollutant. Chromium exists in nature as two main species, the trivalent form, Cr(III), which is relatively innocuous, and the hexavalent form, Cr(VI), considered a more toxic species. At the intracellular level, however, Cr(III) seems to be responsible for most toxic effects of chromium. Cr(VI) is usually present as the oxyanion chromate. Inhibition of sulfate membrane transport and oxidative damage to biomolecules are associated with the toxic effects of chromate in bacteria. Several bacterial mechanisms of resistance to chromate have been reported. The best characterized mechanisms comprise efflux of chromate ions from the cell cytoplasm and reduction of Cr(VI) to Cr(III). Chromate efflux by the ChrA transporter has been established in Pseudomonas aeruginosa and Cupriavidus metallidurans (formerly Alcaligenes eutrophus) and consists of an energy-dependent process driven by the membrane potential. The CHR protein family, which includes putative ChrA orthologs, currently contains about 135 sequences from all three domains of life. Chromate reduction is carried out by chromate reductases from diverse bacterial species generating Cr(III) that may be detoxified by other mechanisms. Most characterized enzymes belong to the widespread NAD(P)H-dependent flavoprotein family of reductases. Several examples of bacterial systems protecting from the oxidative stress caused by chromate have been described. Other mechanisms of bacterial resistance to chromate involve the expression of components of the machinery for repair of DNA damage, and systems related to the homeostasis of iron and sulfur.
铬是一种对微生物和植物来说非必需且广为人知的有毒金属。这种重金属在工业上的广泛使用使其被视为一种严重的环境污染物。铬在自然界中主要以两种形式存在，相对无害的三价形式Cr(III)和毒性更强的六价形式Cr(VI)。然而，在细胞内水平，Cr(III)似乎是铬产生大多数毒性作用的原因。Cr(VI)通常以铬酸根阴离子形式存在。硫酸盐膜转运的抑制以及对生物分子的氧化损伤与铬酸盐在细菌中的毒性作用相关。已经报道了几种细菌对铬酸盐的抗性机制。最具特征的机制包括铬酸根离子从细胞质中流出以及将Cr(VI)还原为Cr(III)。在铜绿假单胞菌和金属贪铜菌（以前称为嗜中性产碱菌）中已证实ChrA转运蛋白介导铬酸盐流出，这是一个由膜电位驱动的能量依赖过程。CHR蛋白家族包括假定的ChrA直系同源物，目前包含来自生命所有三个域大约135个序列。铬酸盐还原由来自不同细菌物种的铬酸盐还原酶进行，产生的Cr(III)可能通过其他机制解毒。大多数已鉴定的酶属于广泛存在的依赖NAD(P)H的黄素蛋白还原酶家族。已经描述了一些细菌系统保护自身免受铬酸盐引起的氧化应激的例子。细菌对铬酸盐的其他抗性机制涉及DNA损伤修复机制成分的表达以及与铁和硫稳态相关的系统。
