Leaves of soybean (Glyxine max. L., var. Progress) were subjected to desiccation, which brought about varying degree of membrane damage as checked with the conductivity method. Progress of injury up to 30% was associated with promotion of ethylene synthesis and with accumulation of 1‐aminocyclopropane‐1‐carboxylic acid (ACC) and 1‐(malonylamino)cyclopropane‐l‐carboxylic acid (MACC) in the cells, as well as with activation of lipoxygenase, the enzyme which is involved in lipid peroxidation and which is capable of forming activated oxygen. The stress‐induced promotion of ethylene synthesis was inhibited by the ACC synthase inhibitor aminooxyacetate (AOA). as well as by n‐propyl gallate (PG), a free radical scavenger and inhibitor of lipoxygenase. Pretreatment of non‐stressed soybean leaves with different concentrations of PG also resulted in the corresponding inhibition of lipoxygenase activity and ethylene formation, the former effect being less pronounced than the latter one. In the tissues pretreated with propyl gallate, the ACC level was not affected, whereas the MACC substantially increased. In leaves showing 40% membrane damage neither lipoxygenase activity nor ethylene synthesis increased any further, despite a further increase in the ACC and MACC levels. Therefore, we propose that there are two prerequisites for effective in vivo synthesis of stress ethylene: promotion of ACC synthesis and activation of a free radical‐generating system, which is responsible for the non‐enzymatic conversion of ACC to ethylene. The latter effect seems to be due to the activation of the membrane‐associated lipoxygenase, which depends on stress‐induced alterations in membrane properties.