Answers are grounded in this paper and cite their sources.
The effects of CO2 on ethylene production rates and on the conversion of 1‐aminocyclopropane‐1‐carboxylic acid (ACC) to ethylene have been investigated in kiwifruit [Actinidia deliciosa (A. Chev.) Liang and Ferguson, cv. Hayward] pericarp tissues. Carbon dioxide concentrations up to 10% notably reduced ethylene production rates but did not affect ACC levels. Carbon dioxide levels from 10 to 28.5% slightly reduced wound‐induced ACC accumulation but resulted in only a slight additional reduction in ethylene production. However, in the presence of saturating amounts of ACC, ethylene formation was stimulated by high CO2: levels. The apparent Vmax and Km for ACC of the in vivo conversion of ACC to ethylene were both increased by high CO2 although to a different extent. When CO2 concentrations were increased from 0.2 to 28.5%, the Vmax varied from 50 to 90 nl g–1 h–1 while the Km for ACC increased from 15 to 72 μM. Thus, the Vmax over Km ratio, which represents the efficiency of ACC conversion to ethylene when ACC concentrations are very low, was reduced by 40% in the presence of 5% CO2 and by 60% in the presence of 28% CO2. The concentrations of ACC, at which ACC, oxidase was inhibited by high CO2 are comparable to the concentrations found in the fruit. It is therefore suggested that the reduction of ethylene production rates in fruits by high CO2 might be exerted at least partially at the level of the conversion of ACC to ethylene.
No takes yet. Share an insight, caveat, or question.
Rothan et al. (1994) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: