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Ethylene production in pear fruit was studied at 2 degrees C. Several observations showed that the inhibiting effect of CO2 on ethylene production did not operate only via the binding site of the ethylene binding protein. Ethylene production of freshly harvested pears was stimulated by 1-methylcyclopropene (1-MCP), but unaffected or inhibited by CO2 which points to different action sites for both molecules. In climacteric pears, where ethylene production was strongly inhibited by 1-MCP, a range of applied CO2 partial pressures was able to inhibit ethylene production further, to an extent similar to untreated pears. In the case of pears that had been stored for a period of 25 weeks, CO2 only had a clear effect after 1-MCP pretreatment. Respiration measurements showed that the effect of CO2 on ethylene production did not operate via an effect on respiration. Ethylene production models based on measurements of whole pears were used to study CO2 effects. Kinetic parameters derived from the models point to the conversion from ACC to ethylene by ACC oxidase as a possible action site for CO2 inhibition.

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The effect of CO2 on ethylene-induced gummosis (secretion of polysaccharides), weight loss and respiration in tulip bulbs (Tulipa gesneriana L.) was investigated. A pretreatment with 1-MCP prevented these ethylene-induced effects, indicating that ethylene action must have been directed via the ethylene receptor. Treatment with 0.3 Pa ethylene for 2 days caused gummosis on 50% of the total number of bulbs of cultivar Apeldoorn, known to be sensitive for gummosis. Addition of CO2 (10 kPa) reduced the ethylene-induced gummosis to 18%. In a second experiment the influence of ethylene and CO2 on respiration and FW loss of bulbs of the cultivar Leen van der Mark was studied. A range of ethylene partial pressures (0.003-0.3 Pa) was applied continuously for 29 days. Ethylene caused a transient peak in O2 consumption rate during the first days after the start of application. The relation between O2 consumption rate and ethylene partial pressure could be described by Michaelis-Menten kinetics. Respiratory peaks were reduced by CO2. This inhibition by CO2 could not totally be due to competition with ethylene at the receptor binding-site, as was indicated by the use of an O2 consumption model. Pre-treatment of bulbs with 1-MCP and subsequent exposure to CO2 showed that CO2 could influence respiration irrespective of any interaction with ethylene. Ethylene and CO2 both stimulated weight loss. The effect of combined treatments of ethylene and CO2 on weight loss was at least as strong as the sum of the separate effects, which implies that competition between ethylene and CO2 at the receptor binding-site was unlikely.