Abstract
The hypersensitive reaction of soybean cuttings to tobacco necrosis virus is characterized by a large stimulation of stress ethylene involving a marked accumulation of free 1-aminocyclopropane-1-carboxylic acid (ACC) and a moderate increase in ethylene-forming enzyme (EFE) activity. The scavengers of hydroxyl radicals (OH) sodium benzoate, sodium formate, mannitol and dimethylsulphoxide, did not affect stress ethylene biosynthesis. Propyl gallate, an inhibitor of lipoxygenase enzymes, substantially reduced the release of stress ethylene from hypersensitive leaves. This reduction was not attributable to an inhibitory effect on EFE activity, but to a strong reduction of free ACC accumulation in leaf tissues. The results suggest that OH and the lipoxygenase system are not involved in stress ethylene produced during the hypersensitive reaction of soybean to this virus.
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