Silicon oxide and sodium silicate were investigated as potential agents for the control of postharvest pink rot in Chinese cantaloupe (cultivar Yujingxing) caused by Trichothecium roseum. In vitro tests showed that sodium silicate, when added to potato dextrose agar, was effective in suppressing the radial growth of the pathogen on the medium, whereas silicon oxide was ineffective. The effectiveness of sodium silicate increased with concentration, and the growth of the fungus was completely inhibited at 100 mm. When melons were dipped in the solutions, both silicon oxide and sodium silicate significantly (P < 0.01) reduced the severity of pink rot of the cantaloupe with lesion diameters reduced by up to fivefold when compared with the controls. Scanning electron microscopy-energy dispersive X-ray analysis showed that silicon (Si)-treated melons had a smoother surface feature and higher Si levels in the epidermis, especially at the stomata and along the junction between the exocarp and mesocarp. Enhanced peroxidase and phenylalanine ammonia lyase activities were observed in sodium-silicate-treated melons but not in those treated with silicon oxide. The results indicate that different mechanisms might be involved in sodium silicate and silicon-oxide-initiated reduction of postharvest pink rot in Chinese cantaloupe.

Among three Hami melon (Cucumis melo L. var. inodorus Jacq.) cultivars (Kalakusai, 8601 and New Queen), there were clear differences in sensitivity to chilling injury (CI) during storage at 22 and 1℃. After 10 weeks storage and 1 week shelf life at 1℃, CI was high in Kalakusai fruit. At 3℃, 8601 fruit developed CI after 7 weeks storage and 1 week shelf life. At 5℃, CI was observed in New Queen fruit after 3 weeks storage and 1 week shelf life. Storage for 10 weeks at 3℃, 7 weeks at 5℃, and 3 weeks at 7℃ resulted in the lowest incidence of decay and the highest percentage of marketable fruit for Kalakusai, 8601 and New Queen melons, respectively. Principal fungi isolated from decayed fruit were Fusarium spp., Alternaria spp., Rhizopus spp., Mucor mucedo and Trichothecium roseum. The fruit held at lower temperature had better appearance, less browning and were firmer.

To investigate how benzo-(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester (BTH) may affect disease resistance of peach fruit (Prunus persica L. cv. Jiubao), harvested fruit were treated with 200 mg/L BTH solution for 5 min immediately after harvest, incubated at 22 ?C and 85-95% RH for 60 h, and then inoculated with Penicillium expansum at a concentration of 1.2×104 conidia per mL. The lesion area and disease-incidence of the BTH-treated fruit were 64.1 and 49.5%, respectively, lower than that of the fruit without BTH-treatment on the 7th day after the inoculation. In the inoculated fruit, the BTH-treatment enhanced the activities of phenylalanine ammonialyase (PAL), polyphenoloxidase (PPO) and peroxidase (POD) as well as the levels of total phenolic compounds and hydrogen peroxide (H2O2), which are considered to play important roles in plant disease resistance. Superoxide dismutase (SOD) activity and ascorbic acid (Vc) level in the inoculated fruit were also enhanced by the BTH treatment during the middle and later periods of the inoculation. The results showed that BTH treatment could significantly enhance the disease resistance of peach fruit after harvest and suggest that postharvest treatment with BTH holds promise as a new technology, substituting for chemical fungicide control of postharvest diseases in fruit.

Postharvest application of harpin to induce resistance was studied in two cultivars of Hami melon (Cucumis melo L. var. inodorus Jacq.) inoculated with Trichothecium roseum. Harpin significantly reduced lesion diameter in inoculated fruit. A greater level of decay control was observed in long-term storage cultivars (cv. 8601). The treatment at 90 mg/L was the most effective concentration and higher concentrations over 90 mg/L failed to promote resistance and did not cause phytotoxicity to melons. Harpin did not demonstrate any fungicide effect in vitro, but suppressed lesion diameter in treated and untreated halves of the same fruit, suggesting induction of local and systemic resistance. Efficacy of suppression lasted 8 and 6 days for '8601' and 5 and 3 days for 'New Queen' cultivars in harpin-treated and untreated halves, respectively. The protection by harpin was associated with the activation of peroxidase (POD) and chitinase (CHT).

Induced resistance was studied in muskmelons (cv. Yindi) inoculated Trichothecium roseurn with postharvest 1,2,3-benzothiadiazole-7-carbothioica cid S-methyl ester (ASM) (100 mg L-1) or harpin (50 mg L-1) treatment. Both ASM and harpin significantly reduced lesion diameter in inoculated fruit. Lesion diameter was limited in the treated and untreated halves of the same fruit, indicating that the local and systemic resistance was induced. Inhibiting efficacy of elicitors lasted 7 and 5 days in the treated and untreated halves. The resistance increased by the chemicals was associated with the activation of peroxidase (POD) and chitinase (CHT). The elicitors induced a significantly and progressively increasing activity of POD and CHT in the treated and untreated halves, and the activation lasted at least 5 days. The activities of POD isoenzymes increased in the treated fruit. However, no new enzyme band was found in the treated and untreated halves.