4.7 Article

Boron-induced amelioration of aluminium toxicity in a monocot and a dicot species

Journal

JOURNAL OF PLANT PHYSIOLOGY
Volume 165, Issue 5, Pages 504-513

Publisher

ELSEVIER GMBH
DOI: 10.1016/j.jplph.2007.03.014

Keywords

aluminium; boron; cell watt; glutathione; root growth

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Previous research has reported inconsistent results from experiments on theinfluence of boron (B) on plant sensitivity to potentially toxic aluminium (AI.) concentrations. Differences in B requirement and cell wall properties among species, especially between Poaceae and dicots, may account for this. This investigation reports amelioration by B of At-induced inhibition of root elongation in At-sensitive cucumber (Cucumis sativus), but not in At-sensitive maize (Zea mays). Vital staining, however, also revealed a positive influence of B supply on At tolerance in maize. In both species, adequate B supply decreased At-induced damage of cell integrity. In cucumber, increasing B supply enhanced At concentrations and haematoxylin staining in root tips. In maize, no differences for root At among B treatments were observed. These results indicate that the positive effect of B on Al. resistance was not due to less At accumulation in root tips. Enhanced concentrations of reduced glutathione were found in roots of At-stressed maize plants growing with adequate B. It is concluded that adequate B supply is essential for prevention of At toxicity in both the dicot and the monocot species. In dicot cucumber, the B-induced amelioration of root elongation, despite higher At accumulation in root tips, indicates B-induced change in either or both Al speciation and compartmentation in the tips. The protection by an adequate B supply of roots against At-induced cell death suggests a role for B in the defence against oxidative stress. This is supported by the observation that At induced enhanced levels of GSH in roots of maize plants growing with adequate B supply but not in those growing with either deficient or excess B concentrations. (c) 2007 Elsevier GmbH. All rights reserved.

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