Oxidative burst and electrolyte leakage induced by sulfhydryl blockers andby membrane permeabilizing reagents in different organs of Egeria densa

Citation
E. Amicucci et al., Oxidative burst and electrolyte leakage induced by sulfhydryl blockers andby membrane permeabilizing reagents in different organs of Egeria densa, PROTOPLASMA, 205(1-4), 1998, pp. 93-100
Citations number
33
Categorie Soggetti
Plant Sciences","Cell & Developmental Biology
Journal title
PROTOPLASMA
ISSN journal
0033183X → ACNP
Volume
205
Issue
1-4
Year of publication
1998
Pages
93 - 100
Database
ISI
SICI code
0033-183X(1998)205:1-4<93:OBAELI>2.0.ZU;2-J
Abstract
Sulfhydryl blockers, such as N-ethylmaleimide, iodoacetate and heavy metals induce a transitory stimulation of Or consumption and H2O2 production (oxi dative burst) and a rapid release of electrolytes in leaves of various aqua tic plants. The correlation between these two responses to N-ethylmaleimide or to Ag+ in separate organs and stages of leaf development was investigat ed in Egeria densa. Only adult leaves were able to respond to the sulfhydry l blockers with an oxidative burst, whereas this response was absent in imm ature growing leaves and in stem and root segments. In N-ethyl maleimide- a s well as in Ag+-treated adult leaves the oxidative burst was constantly as sociated with a relevant electrolyte leakage. These data are consistent wit h a model in which the SH reagent would first interact with a plasmalemma p rotein, leading to an increase in passive permeability to ions and to the a ctivation of an oxidative enzyme of the type of the superoxide synthase des cribed for granulocytes. In its rum, active-oxygen species produced by the activated oxidase might further damage the plasma membrane, increasing its passive permeability. Digitonin and nystatin, two reagents known to cause a permeabilization of lipid membranes, induced in adult E. densa leaves a tr ansient increase in the rate of O-2 consumption and H2O2 production and an electrolyte leakage very similar to those induced by sulfhydryl blockers. T hese effects, however, were nor influenced by the flavin analogues diphenyl ene iodonium and quinacrine, and were partially inhibited by the presence o f CN- and salicylhydroxamic acid, thus suggesting the involvement of a diff erent oxidase in the oxidative burst elicited by these reagents.