Sodium nitroprusside-mediated alleviation of iron deficiency and modulation of antioxidant responses in maize plants.

Abstract

Nitric oxide (NO) has been reported to alleviate Fe-deficiency effects, possibly by enhancing the functional Fe status of plants. This study examines changes in tissue Fe status and oxidative metabolism in Fe-deficient maize (Zea mays L.) plants enriched with NO using sodium nitroprusside (SNP) as a source. Measurements included changes in concentrations of H(2)O(2), non-protein thiols, levels of lipid peroxidation and activities of superoxide dismutase (SOD) and of the Fe-requiring antioxidant haem enzymes catalase, peroxidase and ascorbate peroxidases. Internal NO in Fe-deficient maize plants was manipulated with SNP and the NO scavenger, methylene blue (MB). A key control was treatment with sodium ferrocyanide (SF), a non-NO-supplying analogue of SNP. SNP but not SF caused re-greening of leaves in Fe-deficient maize plants over 10-20 days, increased in vivo NO content, raised chlorophyll and carotenoid concentrations, promoted growth in dry weight, increased the activities of H(2)O(2)-scavenging haem enzymes and enhanced lipid peroxidation, while decreasing SOD activity and H(2)O(2) concentrations. The NO scavenger, MB, blocked the effects of the SNP. Although SNP and SF each donated Fe and increased active Fe, only SNP increased leaf chlorophyll. NO plays a role in Fe nutrition, independently of its effect on total or active Fe status. The most probable mechanism of NO involvement is to increase the intracellular availability of Fe by means of modulating redox. This is likely to be achieved by enhancing the chemical reduction of foliar Fe(III) to Fe(II).