The effects of inhibitors of respiration (KCN and salicylhydroxamic acid, SHAM) and of protein synthesis (cycloheximide and chloramphenicol) on the induction of wound respiration and acid invertase in bisected yam tubers and tissue discs are described. The respiration of tissue discs aged in tris-HCl buffer increases markedly during 3 days following cutting. Respiration is largely insensitive to KCN. Inclusion of KCN or SHAM in the ageing medium inhibits the increase in respiration. Residual respiration is either sensitive to KCN when added to the Warburg vessel (SHAM-aged) or insensitive (KCN-aged). Ageing of discs in KCN + SHAM together, or in the presence of chloramphenicol, totally suppresses the induction of respiration. Ageing in the presence of cycloheximide increases the sensitivity of respiration to KCN. The same inhibitors were also applied to the cut surfaces of bisected, but otherwise intact, tubers for one hour after cutting. The respiration of the tubers increases after bisection, but the total respiration of the tuber halves is unaffected by inhibitor treatment. However, the increase in respiration measured in unaged discs taken from the surface starch/suberin layer is either inhibited (KCN, SHAM and chloramphenicol) or unaffected (cycloheximide) by treatment. The increase in respiration of the periderm is essentially unaffected by the inhibitors except for chloramphenicol which promotes. The induction of acid invertase activity in tissue discs following cutting, is inhibited to a varying degree by all treatments. In contrast, in the starch/suberin layer of bisected yams treated with KCN and/or SHAM the invertase activity is enhanced; chloramphenicol causes some inhibition, but cycloheximide has no effect. The development of invertase in the periderm is reduced by chloramphenicol but is unaffected by other treatments. In all treatments, activity in the corticular tissue (3 cm beneath the cut surface) remains low throughout the healing period. The results may largely be explained by the known metabolic effects caused by these inhibitors.