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Transient Stimulation of Oxygen Uptake Induced by Sulfhydryl Reagents in Egeria densa and Potamogeton crispus Leaves
Author(s) -
Bellando M.,
Sacco S.,
Albergoni F.,
Rocco P.,
Marrè Maria Teresa
Publication year - 1997
Publication title -
botanica acta
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.871
H-Index - 87
eISSN - 1438-8677
pISSN - 0932-8629
DOI - 10.1111/j.1438-8677.1997.tb00654.x
Subject(s) - respiratory burst , dcmu , oligomycin , paraquat , chemistry , biochemistry , respiration , biology , biophysics , photosystem ii , botany , photosynthesis , enzyme , atpase
A vigorous and transient increase of O 2 uptake associated with a simultaneous release of CO 2 was elicited in Egeria densa and in Potamogeton crispus leaves by treatment with N‐ethylmaleimide (NEM) and by other ‐SH group reagents (iodoacetate, p‐(chloromercuri)benzenesulfonate (p‐CMBS), Ag + , Hg 2+ , Cu 2+ ). The NEM‐induced respiratory burst was apparent even in the absence of photosynthesis (darkness, or presence of DCMU) as well as in the presence of the respiration inhibitors cyanide and propyl gallate or SHAM, separate or in combination. In contrast, a complete suppression of the respiratory burst was induced by diphenylene iodonium and by quinacrine, inhibitors of the plasma membrane NADPH oxidase activated in the pathogen‐elicited oxidative burst in granulocytes and in plants. The respiratory burst induced by NEM and by the uncoupler CCCP were additive. The intensity of the respiratory burst was markedly decreased by increasing the pH of the medium from 5 to 8, and partially decreased by the presence of K + in the medium. Azide inhibited the burst (as well as basal respiration) at pH 6.5 but not at pH 5. The stimulation of QO 2 by SH reagents was associated with an early, pronounced membrane depolarization together with a rapid increase of the release into the medium of K + and other electrolytes, and with a rapid decrease of the intracellular ATP, ADP and G6 P contents. The possible relationships between this SH reagent‐induced respiratory burst and the associated effects on E m and electrolyte leakage are discussed.