Intracellular Biotransformation of Cu(II)/Cu(I) Explained High Cu Toxicity to Phytoplankton Chlamydomonas reinhardtii

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

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Author(s)

Detail(s)

Original languageEnglish
Pages (from-to)14772–14781
Journal / PublicationEnvironmental Science and Technology
Volume55
Issue number21
Online published14 Oct 2021
Publication statusPublished - 2 Nov 2021

Abstract

The toxicity of Cu is related to its redox species, but the differential toxicity of Cu(II) and Cu(I) remains unknown. In the present study, we developed a novel protocol to simultaneously detect the biologically produced extracellular Cu(I) and internalized Cu(II) in a freshwater phytoplankton Chlamydomonas reinhardtii. The intracellular Cu(I) was further imaged using a fluorometric probe. Combining these pieces of evidence, we demonstrated that Cu(I) dominated the Cu toxicity in algal cells under Fe-deficient conditions. Our results showed that the labile Cu(I) content increased significantly in the low Fe quota cells. Intracellular biotransformation from Cu(II) to Cu(I) rather than the direct uptake of Cu(I) was responsible for the high Cu toxicity. The abnormal biotransformation from Cu(II) to Cu(I) under Fe deficiency was not resulted from the increase of overall Cu bioaccumulation but was likely due to the change of Cu(II) metabolism. High contents of Cu(II) were accumulated in the normal cells and the low Zn quota cells upon Cu exposure but did not induce cell death, further suggesting that Cu(I) dominated the Cu toxicity to the algae. This is the first study to simultaneously consider the effect of Cu(I) and Cu(II) during Cu exposure in phytoplankton. The results uncovered the underlying mechanisms of high Cu toxicity under Fe deficiency and highlighted the critical role of modulation of Cu metabolism in phytoplankton.

Research Area(s)

  • copper metabolism, cuprous bioimaging, Fe deficiency, intracellular transformation, phytoplankton