To learn how salicylic acid (SA) may affect disease resistance in mango, mango fruit (Mangifera indica L. cv. 'Matisu') were treated with 1 mmol L −1 SA solution under vacuum infiltration for 2 min at a low pressure (−80 kPa) and for an additional 10 min at air pressure. The fruit were inoculated with anthracnose (Colletotichum gloeosporioides Penz.) spore suspension (1 × 10 4 CFU mL −1 ) and incubated at 13 • C, 85-95% RH. Disease incidence and lesion diameter in/on the SA-treated fruit were 37.5% and 20.9% lower than that in/on control fruit on the 4th day of incubation. The study further showed that activities of defensive enzymes in the fruit were significantly enhanced by SA treatment. The activity of phenylalanine ammonia-lyase (PAL) and β-1,3-glucanase in the SA-treated fruit was over 6-or 0.9-fold higher than that in control fruit on the 4th day after the fruit being treated with SA, respectively. Level of hydrogen peroxide (H 2 O 2 ) or superoxide radicals (O 2 − ) generation rate in SA-treated fruit was 22.3% or 79.4% higher than that in controls on the 8th day after the fruit being treated with SA, respectively. These results suggested that PAL and β-1,3-glucanase, as well as H 2 O 2 or O 2 − , may be involved in the enhancement of disease resistance in mango fruit.

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The Ya Li pear (Pyrus bretschneideri) trees were sprayed three times with 2.5 mM salicylic acid (SA) around 30, 60 and 90 days after full flowering. The fruit were harvested at commercial maturity (about 120 days after full flowering), inoculated with Penicillium expansum, and incubated at 20°C, 95-100% RH. The results showed that resistance to the pathogen of the mature pear fruit was remarkably enhanced by the SA sprays. Disease incidence in the SA-treated fruit was 58.0% or 26.5%, and lesion diameter on SA-treated fruit was 58.4% or 29.0% lower than that in/on fruit without SA treatment (control) on day 12 or 17 after incubation, respectively. The SA spray applied to the trees around 30 days after full flowering notably enhanced accumulation of hydrogen peroxide in the young fruit. Meanwhile, activities of defense enzymes, including peroxidase, phenylalanine ammonia-lyase (PAL), chitinase or b-1,3-glucanase in the young fruit from SA-treated trees was 29.5%, 60.0%, 24.4% or 35.7% higher than that in the control fruit 4 days after the SA spraying. Furthermore, after harvest, activities of PAL, chitinase and b-1,3-glucanase were still significantly higher in the mature pear fruit from the trees sprayed three times with SA than those of the control fruit. Activities of the antioxidant enzymes including catalase and ascorbate peroxidase in the young fruit were significantly reduced by SA spraying. However, the activity of another antioxidant enzyme, glutathione reductase in the young fruit was significantly enhanced by SA spraying. These results suggest that enzymes exerting their functions in different ways may be coordinately regulated by SA in the pear fruit. Our study indicates that treatment of SA sprays on the trees may provide further protection against postharvest disease of Ya Li pear fruit in practice and could be used as an alternative and economical approach to reduce application of chemical fungicides.