Environmental & Life Sciences, Trent University, Peterborough, Ontario, Canada.
Environ Toxicol Chem. 2011 Feb;30(2):469-76. doi: 10.1002/etc.392.
Phytochelatins (PCs) are short metal detoxification peptides made from the sulfur-rich molecule glutathione. The production of PCs by algae caused by Se exposure has never been studied, although many algae accumulate Se, forming Se-rich proteins and peptides, and higher plants have demonstrated PC production when treated with Se; therefore, a goal of the current study was to examine whether Se induces PC production in algae. Furthermore, selenate is thought to compete with sulfate in the S assimilation pathway, and sulfate therefore may have a protective effect against the toxic effects of high doses of Se in algae. Hence, the interaction of selenate and sulfate was investigated with respect to the induction of PCs. Chlorella vulgaris was cultured in media with either low (31.2 µM) or high (312 µM) concentrations of sulfate. These cultures were exposed to selenate in doses of 7, 35, and 70 nM for 48 h. In a separate treatment, Cd (890 nM) was added as a positive PC-inducing control, and one no-metal negative control was used. Total Se and Se speciation were determined, and glutathione, phytochelatin-2, and phytochelatin-3 were quantified in each of cell digests, cell medium, and cell lysates. We found that PCs and their precursor glutathione were induced by selenate as well as by a Cd control. The high concentration of sulfate was able to counter selenate-induced production of PCs and glutathione. These data support two possible mechanisms: a negative feedback system in the S assimilation pathway that affects PC production when sulfate is abundant, and competition for uptake at the ion transport level between selenate and sulfate.
植物螯合肽（PCs）是由富含硫的分子谷胱甘肽制成的短金属解毒肽。尽管许多藻类积累硒，形成富含硒的蛋白质和肽，但藻类暴露于硒时产生 PCs 的情况从未被研究过，而且高等植物在用硒处理时已证明能够产生 PC；因此，目前研究的一个目标是检查硒是否会诱导藻类产生 PC。此外，人们认为硒酸盐会与硫酸盐在 S 同化途径中竞争，因此硫酸盐可能对藻类中高剂量硒的毒性有保护作用。因此，研究了硒酸盐和硫酸盐之间的相互作用，以了解它们对 PCs 的诱导作用。小球藻在含有低（31.2 µM）或高（312 µM）浓度硫酸盐的培养基中培养。这些培养物分别用 7、35 和 70 nM 的硒酸盐处理 48 h。在另一种处理中，添加 Cd（890 nM）作为阳性 PC 诱导对照，使用一个无金属阴性对照。测定总硒和硒形态，定量测定每个细胞消化物、细胞培养基和细胞裂解物中的谷胱甘肽、PC-2 和 PC-3。我们发现 PCs 及其前体谷胱甘肽是由硒酸盐以及 Cd 对照诱导的。高浓度的硫酸盐能够抵消硒酸盐诱导的 PCs 和谷胱甘肽的产生。这些数据支持两种可能的机制：一种是 S 同化途径中的负反馈系统，当硫酸盐丰富时会影响 PC 的产生，另一种是硒酸盐和硫酸盐在离子转运水平上的竞争。
