Effect Of Interaction Between 1-mcp And Internal Ethylene On Ripening Physiology Of Tomato And Avocado Fruit

Using tomato (Solanum lycopersicum L. cv. Sebring and Florida 47) and avocaodo (Persea Americana L. cv. Booth 7) fruit as a model system, this study tested the idea that internal ethylene levels can modulate the efficacy of 1-MCP at suppressing ripening in climacteric fruits. The main results were exhibited as follows:1. Breaker tomato (cv. Sebring) fruit were treated with gaseous 1-MCP (SmartFreshSM Quality System) under conditions (516 nL L^-1) affording maximum inhibition of ripening, followed by subsequent exposure to 100μL^-1 ethylene for 3 or 6 h. Fruit softening and hue angle decline in 1-MCP-treated fruit were minimally affected in response to ethylene。In contrast to sequential 1-MCP and ethylene treatments, simultaneous treatment of breaker'Sebring'tomato fruit with 100μL L^-1 ethylene and gaseous 500 nL L^-1 1-MCP completely negated the capacity of 1-MCP to inhibit fruit softening and hue angle decline. When breaker fruit were treated with 100μL L ^-1 ethylene for 6 h followed by exposure to aqueous 1-MCP (200μg L^-1), sensitivity to 1-MCP was significantly reduced in the short-term (0–1 h) and recovered within 6 h to patterns characteristic of fruit receiving 200μg L^-1 aqueous 1-MCP without prior exposure to ethylene. Re-sensitization was reflected in patterns of softening, climacteric ethylene and respiratory responses, hue angle decline, lycopene content, titratable acidity and total phenolic content changes. The time required for re-sensitization to 1-MCP paralleled the time required for return of internal ethylene levels to concentrations present prior to ethylene treatment.2. Breaker and pink'Florida 47'tomato fruit were subjected to hypobaria hypoxic (HH) (8 kPa, 1.7 kPa O2) for 6 h, followed by treatment at ambient pressure with aqueous 1-MCP at a sub-saturating dose (50μg L^-1) and exposure duration (1 min). Immediately following HH, breaker and pink fruit had a 76% and 62% lower IEC, 66% and 60% lower ACO activities, respectively, as well as enhanced sensitivity to 1-MCP compared with fruit not receiving HH. Increased sensitivity to 1-MCP was evident in further suppression of fruit firmness and hue angle declines, and delayed peak ethylene production. Within 3 h of removal of fruit from HH, IEC and ACO activity had returned to pre-HH values and responses to 1-MCP were comparable with those of fruit receiving 1-MCP without prior HH. Decreased IEC and increased sensitivity to 1-MCP in response to HH were also observed for fruit at more advanced ripening (pink stage). We addressed whether increased sensitivity to 1-MCP following exposure to HH was a response to reduced pO2. For this objective, breaker and pink fruit were exposed to hypobaria normoxic (HN) (21.3 kPa, 21.3 kPaO2) for 6 h prior to treatment with 50μg L?1 aqueous 1-MCP. The results showed that IEC, ACO activity and responsiveness to 1-MCP were unaffected in fruit following exposure to HN, indicating that enhanced sensitivity to 1-MCP following HH is a result of low pO2-mediated reductions in IEC.3. The immediate treatment with 1- MCP after HH (8 kPa, 1.7 kPa O2) also more evidently affected the activity trends of cell wall enzymes including polygalacturonase (PG), cellulase (Cx) pectinmethylesterase (PME),α-galactosidase (α-Gal) activity, typically on PG activity. Consistent with trend of PG activity, water/CDTA-soluble uronic acid (UA) content were more strongly suppressed by treatment of 50μg L^-1 1-MCP following HH, compared with 1-MCP treatment without prior to HH; Polyuronides in fruit treated with 1-MCP following HH exhibited slower molecular mass downshifts compared with the control and 1-MCP- treated fruit. In addition, all results in this study showed that there was no significant difference between control and HH treatment.4. The role of IEC in modulating 1-MCP responsiveness was further tested using avocado, a fruit that accumulates markedly higher IEC compared with tomato fruit. Preclimacteric (1 d after harvest)'Booth 7'avocado fruit were treated for 1 min with aqueous 1-MCP at 100 and 500μg L^-1. Both concentrations strongly suppressed softening, and delayed climacteric ethylene production and respiration maxima. Mid-climacteric fruit (7 d after harvest) showed complete loss of or diminished sensitivity to 1-MCP at 100 and 500μg L^-1, respectively. Application of higher dose of aqueous 1-MCP (2500μg L^-1) revealed that softening, respiration and ethylene production of mid-climacteric avocado remained highly sensitive to inhibition of ethylene perception. In experiments testing the effects of reducing IEC on 1-MCP responses, mid-climacteric (d 6.5) avocado were exposed to hypoxia (2 kPa O2) for 12 h, followed by exposure to aqueous 1-MCP at 1000μg L^-1. IEC prior to hypoxia averaged about 38.6μL L^-1. IEC following exposure to air or hypoxia for 12 h averaged around 54 and 16μL L^-1, respectively. Fruit treated with 1000μg L^-11-MCP following hypoxia showed greater suppression of fruit softening, and further delays in peak ethylene production and respiration compared with fruit treated with 1-MCP alone. 1-MCP and low O2+1-MCP treatments applied to mid-climacteric fruit also delayed PG accumulation and depolymerization of polyuronides, indicating that cell wall metabolism in avocado fruit remains ethylene sensitive through advanced ripening. Possible mechanisms by which 1-MCP sensitivity is modulated by ethylene are discussed.In summary, we propose that internal ethylene levels may contribute to the divergent sensitivities of some climacteric fruits to 1-MCP applied after initiation of ripening.