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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

Maria Teresa Marrè*, Enrica Amicucci, Luisa Zingarelli, Francesco Albergoni, and Erasmo Marrè

Centro di Studio del Consiglio Nazionale delle Ricerche sulla Biologia Cellulare e Molecolare delle Piante, via Celoria 26, 20133 Milan, Italy (M.T.M.); and Dipartimento di Biologia, Università di Milano, via Celoria 26, 20133 Milan, Italy (E.A., L.Z., F.A., E.M.)

In leaves of Egeria densa Planchon, N-ethylmaleimide (NEM) and other sulfhydryl-binding reagents induce a temporary increase in nonmitochondrial respiration (Delta QO2) 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 Delta QO2 was associated with H2O2 production and both effects depended on the presence of external Ca2+; (b) Ca2+ influx was markedly increased by treatment with NEM; (c) the Ca2+ channel blocker LaCl3 inhibited Delta QO2, electrolyte release, and membrane depolarization induced by the sulfhydryl reagents; and (d) LaCl3 also inhibited electrolyte leakage induced by the direct infiltration of the leaves with H2O2. 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 Ca2+ 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.

1   This work was supported in part by the Ministero Italiano dell' Università e della Ricerca Scientifica e Tecnologica.
*   Corresponding author; e-mail teamarre{at}imiucca.unimi.it; fax 39-2-26604399.

Plant Physiol. (1998) 118: 1379-1387
Copyright Clearance Center:   0032-0889/98/118//09
© 1998 American Society of Plant Physiologists




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