Ethylene and wound‐induced cyanide‐resistant respiration climaxes in potato: The synergistic role of CO₂ and the selective role of lycorine

Abstract

When treated with ethylene in O2, conditioned potato (Solanum tuberosum L. cv. Russet Burbank) tubers – that is, tubers kept at room temperature for 10 days or more – yield slices that are CN− resistant. Ten % CO2 in the gas mixture not only synergizes the effect of ethylene, but replaces the need for conditioning as well. The response to CO2 is more pronounced with increasing time from harvest. By contrast fresh slices from untreated tubers are CN− sensitive, as are slices from tubers incubated in O2 or O2 plus CO2. The suggestion is made that CN− resistance is constitutive, and that treatment with ethylene/CO2 in O2 confers on potato tuber tissue a resistance to the extensive degradation of membrane phospholipids that normally attends slicing and leads to the loss of CN− resistance. In this connection respiration inhibition by imidazole, an inhibitor of fatty acid α‐oxidation, is extensive in slices of untreated tubers, and sharply diminished in slices of ethylene‐treated tubers in proportion to their CN− resistance. The coextensive rise of respiration rate and CN− resistance in aged potato slices has led to the presumption that the CN−‐resistant path mediates the respiration climax. Accordingly the alkaloid, lycorine, has been considered to inhibit the development of CN− resistance in aging potato slices because it curtails the wound‐induced respiration. A comparison was carried out on the effect of lycorine on CN−‐sensitive and CN−‐resistant fresh slices – the latter obtained from ethylene/CO2‐treated tubers. Lycorine suppressed the development of the wound‐induced respiration without restricting the development of CN− resistance.

Interaction of ethylene and CO2

“…One appears to be an ethyleneinduced respiration rise in intact tubers. In tissue slices the mixture of ethyiene, O2 and CO2 appears to prevent the loss of the alternate respiratory pathway, perhaps by inhibiting the breakdown of membranes (Laties 1987).…”