Stress Ethylene does not Originate Directly from Lipid Peroxidation during Chilling-Enhanced Photooxidation

Abstract

Summary Stress ethylene synthesis was monitored in detached cucumber ( Cucumis sativus ) leaves under conditions (5 °C and 1000μtEinstein m −2 s −1 ) that promote lipid peroxidation. Previous work has shown that such a chilling and light stress in detached cucumber leaves causes superoxide anion radical and singlet oxygen production and is accompanied by pigment bleaching, loss of endogenous antioxidants, ultrastructural damage and ethane generation due to lipid peroxidation [Wise, R. R. and A. W. Naylor: Plant Physiol. 83, 272–278 and 278–282 (1987a, b)]. In spite of the considerable light- and chilling-enhanced lipid peroxidation, as evidenced by ethane generation, all of our observations of ethylene production in the experiments described here indicate that the S-adenosylmethionine (SAM) → 1-aminocyclopropane-1-carboxylic acid (ACC) → C 2 H 4 enzymatic pathway was the chief, if not the sole, source of ethylene. When ethane generation was inhibited in leaves by atrazine (which blocked superoxide radical-dependent lipid peroxidation), ethylene production was unaffected. The complete photobleaching at room temperature of isolated cucumber thylakoids resulted in substantial amounts of ethane, but no detectable ethylene. The Q 10 temperature coefficient for ethylene generation was 1.6, within the range which is typical for enzymatic reactions. Ethylene generation was significantly, but not completely, inhibited by CoCl 2 or aminoethoxyvinyl glycine, known inhibitors of enzymatic ethylene biosynthesis. The well-established SAM → ACC → C 2 H 4 biosynthetic pathway was apparently fully engaged in the detached cucumber leaves while lipid peroxidation contributed insignificantly to stress ethylene production.