Jacks of metal/metalloid chelation trade in plants-an overview

Abstract

Varied environmental compartments including soils are being contaminated by a myriad toxic metal(loid)s (hereafter termed as "metal/s") mainly through anthropogenic activities. These metals may contaminate food chain and bring irreparable consequences in human. Plant-based approach (phytoremediation) stands second to none among bioremediation technologies meant for sustainable cleanup of soils/sites with metal-contamination. In turn, the capacity of plants to tolerate potential consequences caused by the extracted/accumulated metals decides the effectiveness and success of phytoremediation system. Chelation is among the potential mechanisms that largely govern metal-tolerance in plant cells by maintaining low concentrations of free metals in cytoplasm. Metal-chelation can be performed by compounds of both thiol origin (such as GSH, glutathione; PCs, phytochelatins; MTs, metallothioneins) and non-thiol origin (such as histidine, nicotianamine, organic acids). This paper presents an appraisal of recent reports on both thiol and non-thiol compounds in an effort to shed light on the significance of these compounds in plant-metal tolerance, as well as to provide scientific clues for the advancement of metal-phytoextraction strategies.

Keywords: chelation; glutathione; metal/metalloids; metallothioneins; organic acid; phytochelatins; plant tolerance; thiol compounds.

Figure 1

Major thiol- (A) and non-thiol compounds (B) involved in the chelation/detoxification of metal(loid)s in plants.

Figure 2

Schematic representation of major functions, interrelationships among thiol and non-thiol compounds, and their coordination with other defense system components in metal(loid)-exposed plants. As discussed in the text, plant responses to heavy metals include: (A) metal ion binding to the cell wall and root exudates; (B) reduction of metal influx across the plasma membrane; (C) membrane efflux pumping into the apoplast (ATP-binding-cassette (ABC) and P_1B-ATPase transporter); (D) heavy metal (HM) chelation in the cytosol by ligands such as phytochelatins (PC), metallothioneins (MT), organic acids, and amino acids; (E) ROS defense mechanism [Antioxidant enzymes (SOD: superoxide dismutase, CAT: catalase, APX: ascorbate peroxidase, GPX: glutathione peroxidase, GSH: glutathione reduce and GSSG: glutathione oxidase)]; (F) hormone signaling pathway. (G) Transport and compartmentalization in the vacuole (ABC and P1B-ATPase transporter, NRAMP: natural resistance associated macrophage protein, CAX: cation/proton exchanger). Metal ions are shown as black dots.