Is acetaldehyde the causal agent in the retardation of carnation flower senescence by ethanol?

A 3% ethanol holding solution inhibits the conversion of 1-aminocyclopropane-1-carboxylic acid (ACC) to ethylene, and doubles the vase-life of cut carnation flowers. Although the most effective concentration varies during experimentation, high concentrations of ethanol have negative effects. The most pronounced of these is the death of the ovary. Ethanol levels are much higher in the ovaries of treated flowers, than control flowers. A large amount of acetaldehyde was detected in the ovaries of treated flowers. Acetaldehyde was also detected in all other floral organs tested. Acetaldehyde is present in the head-space surrounding ethanol treated flowers, but not control flowers. This indicates that some of the ethanol applied as a post-harvest treatment is broken down to acetaldehyde, within the plant tissue, and released into the micro-atmosphere by the flower. If the conversion of ethanol to acetaldehyde is impeded, using an inhibitor of alcohol dehydrogenase, 4-methyl pyrazole, ethanol is no longer effective. Acetaldehyde, (1 and 3 %), as a holding solution, gave similar results as a 3 % ethanol holding solution. It appears that acetaldehyde, produced from ethanol, is the causal agent for the retardation of carnation flower senescence.