Microbial siderophores and root exudates enhanced goethite dissolution and Fe/As uptake by As-hyperaccumulator Pteris vittata.

Environ Pollut

State Key Lab of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Jiangsu 210023, People's Republic of China; Horticultural Sciences Department, University of Florida, Gainesville, FL 32611, United States. Electronic address:

Published: April 2017

Arsenic (As) in soils is often adsorbed on Fe-(hydro)oxides surface, rendering them more resistant to dissolution, which is undesirable for phytoremediation of As-contaminated soils. Arsenic hyperaccumulator Pteris vittata prefers to grow in calcareous soils where available Fe and As are low. To elucidate its mechanisms of acquiring Fe and As from insoluble sources in soils, we investigated dissolution of goethite with pre-adsorbed arsenate (AsV; As-goethite) in presence of four organic ligands, including two root exudates (oxalate and phytate, dominant in P. vittata) and two microbial siderophores (PG12-siderophore and desferrioxamine B). Their presence increased As solubilization from As-goethite from 0.03 to 0.27-5.33 mg L compared to the control. The siderophore/phytate bi-ligand treatment released 7.42 mg L soluble Fe, which was 1.2-fold that of the sum of siderophore and phytate, showing a synergy in promoting As-goethite dissolution. In the ligand-mineral-plant system, siderophore/phytate was most effective in releasing As and Fe from As-goethite. Moreover, the continuous plant uptake induced more As-goethite dissolution. The continued release of As and Fe significantly enhanced their plant uptake (from 0.01 to 0.43 mg plant As and 2.7-14.8 mg plant Fe) and plant growth (from 1.2 to 3.1 g plant fw) in P. vittata. Since microbial siderophores and root exudates often coexist in soil rhizosphere, their synergy in enhancing dissolution of insoluble As-Fe minerals may play an important role in efficient phytoremediation of As-contaminated soils.

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Source
http://dx.doi.org/10.1016/j.envpol.2017.01.016DOI Listing

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