The Respiratory Burst and Electrolyte Leakage Induced by Sulfhydryl Blockers in Egeria densa Leaves Are Associated with H2O2 Production and Are Dependent on Ca2+ Influx1

In leaves of Egeria densa Planchon, N -ethylmaleimide (NEM) and other sulfhydryl-binding reagents induce a temporary increase in nonmitochondrial respiration (ΔQO 2 ) that is inhibited by diphenylene iodonium and quinacrine, two known inhibitors of the plasma membrane NADPH oxidase, and are associat...

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Published inPlant physiology (Bethesda) Vol. 118; no. 4; pp. 1379 - 1387
Main Authors Marrè, Maria Teresa, Amicucci, Enrica, Zingarelli, Luisa, Albergoni, Francesco, Marrè, Erasmo
Format Journal Article
LanguageEnglish
Published American Society of Plant Physiologists 01.12.1998
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Summary:In leaves of Egeria densa Planchon, N -ethylmaleimide (NEM) and other sulfhydryl-binding reagents induce a temporary increase in nonmitochondrial respiration (ΔQO 2 ) that is inhibited by diphenylene iodonium and quinacrine, two known inhibitors of the plasma membrane NADPH oxidase, and are associated with a relevant increase in electrolyte leakage (M. Bellando, S. Sacco, F. Albergoni, P. Rocco, M.T. Marré [1997] Bot Acta 110: 388–394). In this paper we report data indicating further analogies between the oxidative burst induced by sulfhydryl blockers in E. densa and that induced by pathogen-derived elicitors in animal and plant cells: (a) NEM- and Ag + -induced ΔQO 2 was associated with H 2 O 2 production and both effects depended on the presence of external Ca 2+ ; (b) Ca 2+ influx was markedly increased by treatment with NEM; (c) the Ca 2+ channel blocker LaCl 3 inhibited ΔQO 2 , electrolyte release, and membrane depolarization induced by the sulfhydryl reagents; and (d) LaCl 3 also inhibited electrolyte leakage induced by the direct infiltration of the leaves with H 2 O 2 . These results suggest a model in which the interaction of sulfhydryl blockers with sulfhydryl groups of cell components would primarily induce an increase in the Ca 2+ cytosolic concentration, followed by membrane depolarization and activation of a plasma membrane NADPH oxidase. This latter effect, producing active oxygen species, might further influence plasma membrane permeability, leading to the massive release of electrolytes from the tissue.
Bibliography:Corresponding author; e-mail teamarre@imiucca.unimi.it; fax 39–2–26604399.
ISSN:0032-0889
1532-2548