Metal uptake and detoxification mechanisms in Erica andevalensis growing in a pyrite mine tailing

Erica andevalensis was found growing in the banks of extremely acidic, heavily metal-contaminated tailings of an abandoned pyrite mine in the Mértola region of southeastern Portugal. Elemental analysis by ICP-AES and AAS showed that Al and Fe, quantitatively the two principal contaminants of the pla...

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Published inEnvironmental and experimental botany Vol. 61; no. 2; pp. 117 - 123
Main Authors Turnau, Katarzyna, Henriques, Fernando S., Anielska, Teresa, Renker, Carsten, Buscot, François
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 01.11.2007
Elsevier Science
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Summary:Erica andevalensis was found growing in the banks of extremely acidic, heavily metal-contaminated tailings of an abandoned pyrite mine in the Mértola region of southeastern Portugal. Elemental analysis by ICP-AES and AAS showed that Al and Fe, quantitatively the two principal contaminants of the plant's substrate, accumulated in the plant, reaching average concentrations of 1745 (±81) and 2328 (±745) mg kg −1 of leaf dry weight, respectively. Quantitative EDX-analysis of the spatial distribution of these elements within the roots and shoots of E. andevalensis revealed that they were predominantly detected in the cell walls of epidermal tissues, as well as in leaf glandular hairs. This finding indicates that sequestration of Al and Fe in the extracellular matrix of protective tissues, away from the internal parenchymas, constitutes an important detoxification mechanism. Si was always found to co-localize with Al and Fe, which would support its proposed role in alleviating metal toxicity. Hymenoschyphus ericae was identified as the fungal endosymbiont of Erica roots and both its extra- and intraradical mycelia accumulated exceedingly high metal levels, thus effectively contributing to reduce metal availability for the plant. It is concluded that E. andevalensis works with its fungal partners to exclude contaminating metals from intracellular sites where they could disrupt normal cell functioning.
Bibliography:http://dx.doi.org/10.1016/j.envexpbot.2007.05.001
ObjectType-Article-2
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ISSN:0098-8472
1873-7307
DOI:10.1016/j.envexpbot.2007.05.001