Heavy Metal Induction of Ethylene Production and Stress Enzymes. I. Kinetics of the Responses

Abstract

In higher plants metal toxicity affects several physiological and biochemical processes. However, the primary target of metal action at the cellular level might be the plasmamembrane since this is the first functional structure encountered by a metal when it penetrates into the cell. Progressive membrane desintegration, leading to enhanced permeability and to loss of membrane function, is observed during senescence (Thompson 1988). Increasing evidence becomes available that various stress factors (drought, chilling, injury, ozone, UV-B, heavy metals, salinity, etc.) induce responses at the cellular level, analogous to those observed during senescence (McKersie et al. 1988, Noodén 1988). Membrane destabilization always appears to be involved. It is attributed to lipid peroxidation, due to an enhanced production of highly toxic oxygen free radicals. Metals (Cu, Fe, Hg, etc.), which perform one electron oxidoreduction reactions in solutions, easily produce free radicals. These radicals are also involved in the lipoxygenase (LOX) mediated oxidation of polyunsaturated fatty acids. Oxygen free radicals and hydroperoxides, generated by LOX, might stimulate the conversion of ACC into ethylene. There is at least indirect evidence that ethylene may facilitate the peroxidative pathway leading to membrane destabilization (Thompson et al. 1982).