Biogeochemistry Division, Institute of Radiochemistry, Helmholtz-Zentrum Dresden-Rossendorf eV, Dresden, Germany.
Biometals. 2011 Dec;24(6):1197-204. doi: 10.1007/s10534-011-9478-6. Epub 2011 Jul 14.
Uranium (U) as a redox-active heavy metal can cause various redox imbalances in plant cells. Measurements of the cellular glutathione/glutathione disulfide (GSH/GSSG) by HPLC after cellular U contact revealed an interference with this essential redox couple. The GSH content remained unaffected by 10 μM U whereas the GSSG level immediately increased. In contrast, higher U concentrations (50 μM) drastically raised both forms. Using the Nernst equation, it was possible to calculate the half-cell reduction potential of 2GSH/GSSG. In case of lower U contents the cellular redox environment shifted towards more oxidizing conditions whereas the opposite effect was obtained by higher U contents. This indicates that U contact causes a consumption of reduced redox equivalents. Artificial depletion of GSH by chlorodinitrobenzene and measuring the cellular reducing capacity by tetrazolium salt reduction underlined the strong requirement of reduced redox equivalents. An additional element of cellular U detoxification mechanisms is the complex formation between the heavy metal and carboxylic functionalities of GSH. Because two GSH molecules catalyze electron transfers each with one electron forming a dimer (GSSG) two UO(2) (2+) are reduced to each UO(2) (+) by unbound redox sensitive sulfhydryl moieties. UO(2) (+) subsequently disproportionates to UO(2) (2+) and U(4+). This explains that in vitro experiments revealed a reduction to U(IV) of only around 33% of initial U(VI). Cellular U(IV) was transiently detected with the highest level after 2 h of U contact. Hence, it can be proposed that these reducing processes are an important element of defense reactions induced by this heavy metal.
铀（U）作为一种氧化还原活性重金属，会在植物细胞中引起各种氧化还原失衡。细胞接触 U 后通过 HPLC 测量细胞内的谷胱甘肽/谷胱甘肽二硫化物（GSH/GSSG），结果显示该物质对这个基本氧化还原对有干扰。10μM U 接触不影响 GSH 含量，而 GSSG 水平立即增加。相比之下，更高的 U 浓度（50μM）则大大提高了这两种形式的含量。通过 Nernst 方程，可以计算出 2GSH/GSSG 的半细胞还原电位。在 U 含量较低的情况下，细胞内氧化还原环境向更氧化的条件转变，而较高的 U 含量则产生相反的效果。这表明 U 接触会消耗还原的氧化还原当量。用氯代二硝基苯人工耗尽 GSH，并通过四唑盐还原测量细胞的还原能力，强调了对还原氧化还原当量的强烈需求。细胞 U 解毒机制的另一个要素是重金属与 GSH 的羧酸功能基之间的络合。由于两个 GSH 分子每个分子都用一个电子催化电子转移，形成二聚体（GSSG），因此两个 UO2(2+)被未结合的氧化还原敏感巯基部分还原为每个 UO2(+)。随后 UO2(+)歧化为 UO2(2+)和 U(4+)。这解释了为什么体外实验显示只有约 33%的初始 U(VI)被还原为 U(IV)。在接触 U 2 小时后，细胞内 U(IV)的水平达到最高，短暂检测到。因此，可以提出这些还原过程是由这种重金属诱导的防御反应的重要组成部分。
