Blast resistance induced in rice by some phthalocyanine metal complexes. Implication of active oxygen

被引:0
作者
Aver'yanov, AA
Lapikova, VP
Novodarova, GN
Krainova, NY
Gaivoronskaya, LM
机构
来源
MODERN FUNGICIDES AND ANTIFUNGAL COMPOUNDS II | 1999年
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中图分类号
S3 [农学(农艺学)];
学科分类号
0901 ;
摘要
Synthetic phthalocyanine metal complexes (PCMC) were studied. Some of them possessed redox reactions in the dark yielding superoxide and hydroxyl free radicals. Several PCMC exhibited the light-independent and light-induced toxicity to Magnaporthe grisea, the causal fungus of the rice blast disease. Both kinds of antifungal action were diminished, more or less, by antioxidant reagents detoxifying those free radicals and other active oxygen (AO) species. Some PCMC (including nontoxic ones), in contact with a leaf of the blast-susceptible rice cultivar, rendered leaf diffusates fungitoxic. This property was stimulated by illumination and inhibited by antioxidant reagents. When added to inocula, PCMC suppressed the blast occurrence in correlation with a level of the leaf diffusate toxicity. Seed treatment with 1 mu g/ml PCMC induced the disease resistance in seedlings as late as 4 weeks after the treatment. In this case, diffusates of healthy and, especially, infected leaves acquired the additional light-stimulated, AO-dependent toxicity. Hypersensitive necrotic spots were frequent at infection sites of treated plants in contrast to infected untreated or to healthy treated counterparts. A rice callus culture underwent necrotisation only in the simultaneous presence of the fungal elicitor and PCMC. As well, the two agents induced a fungitoxicity of callus diffusates, most strong under the dual treatment. It points out a synergism between PCMC and fungal infection in the induction of the antifungal responses. Both the necrotisation and the toxicity were diminished by the antioxidant reagents. It is suggested that PCMC prompted the AO generation in treated plants systemically and potentiated cells for a local hypersensitive necrosis in response to infection challenge. These reactions appear to contribute to the acquired disease resistance.
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页码:389 / 395
页数:7
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