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Title

Activated oxygen and antioxidant defences in iron-deficient pea plants

AuthorsIturbe-Ormaetxe, Iñaki ; Morán, José F. ; Arrese-Igor, César; Gogorcena Aoiz, Yolanda ; Klucas, R. V.; Becana Ausejo, Manuel
KeywordsPisum sativum
antioxidants
Fenton reaction
free radicals
iron deficiency
mineral nutrition
Issue DateApr-1995
PublisherJohn Wiley & Sons
CitationPlant Cell and Environment 18 (4): 421–429 (1995)
AbstractIron (Fe) deficiency in pea leaves caused a large decrease (44–62&) in chlorophyll a, chlorophyll b and carotenoids, and smaller decreases in soluble protein (18&) and net photosynthesis (28&). Catalase, non-specific peroxidase and ascorbate peroxidase activities declined by 51& in young Fe-deficient leaves, whereas monodehydroascorbate reductase, dehydroascorbate reductase and glutathione reductase activities remained unaffected. Ascorbate peroxidase activity was highly correlated (r2= 0. 99, P < 0. 001) with the Fe content of leaves, which allows its use as an indicator of the Fe nutritional status of the plant. Fe deficiency resulted in an increase of CuZn-superoxide dismutase but not of Mn-superoxide dismutase. The content of ascorbate decreased by only 24& and those of reduced and oxidized glutathione and vitamin E did not vary. The low-molecular-mass fraction of Fe-sufficient leaves contained 30–65 μg (g dry weight)−1 Mn. This concentration was 15–60 times greater than that of Fe and Cu in the same fraction, and was further enhanced (1. 5- to 2. 5-fold) by Fe deficiency without causing Mn toxicity. The concentration of catalytic Fe, that is, of Fe active for free radical generation, was virtually zero and that of catalytic Cu did not change with severe Fe deficiency. Because catalytic metals mediate lipid and protein oxidation in vivo, the above findings would explain why oxidatively damaged lipids and proteins do not accumulate in Fe-deficient leaves.
Description22 Pags. The definitive version, with Figs. and Tabls., is available at: http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-3040
Publisher version (URL)http://dx.doi.org/10.1111/j.1365-3040.1995.tb00376.x
URIhttp://hdl.handle.net/10261/109121
DOI10.1111/j.1365-3040.1995.tb00376.x
ISSN0140-7791
E-ISSN1365-3040
Appears in Collections:(EEAD) Artículos
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