Physiological response of adult Salix aurita in wetland vegetation affected by flooding with As-rich fine pyrite particles.

ABSTRACT

An uncontrolled, natural episode of flooding with waters contaminated with As-rich pyrite (FeAsS) particles caused serious ecological damage leading to necrosis of plants growing in a fresh wet meadow located in an area characterized by unique geological structures rich in arsenopyrites. One of the few plant species capable of surviving this event was Salix aurita L., which grew in numbers in the analyzed area, but individual plants were affected differently by toxic flooding. No significant phenotypic changes (Group I), through partial leaf and/or stem necrosis (Group II) up to necrosis of the whole parental plant and root suckers (Group III), were observed for various willow clumps. These varied phenotypic responses of S. aurita to As-rich sediments were compared with the biochemical status of the foliage of willow trees, and with their rhizosphere physiological parameters. Our in situ study revealed that the biochemical status of leaves reflects the phenotypic damage incurred by adult willows growing in their natural environment and affected by the flooding. In leaves of willows with increasingly negative phenotypic changes (Groups I → II → III) as well as increasing levels of reactive oxygen species, malondialdehyde and decreased levels of glutathione and thiol groups were detected. Phytochelatins, commonly considered major As chelators, were not detected in S. aurita leaves. Despite a decrease in the size of leaves with the intensity of tree damage, all leaves expressed a normal level of leaf pigments. Phenotypic changes observed for particular willow clumps were only partly related to soil As levels. Moreover, As and S (but not Fe) foliar levels were related but did not correspond strictly with foliar biochemical features, or with soil As levels, soil pH or soil microbial activity, with the latter two drastically decreased in the rhizospheres of willows from Groups II and III.