嘧菌酯及SHAM对4种植物病原真菌的活性和作用方式研究

Activity of Azoxystrobin and SHAM of Four Plant Pathogens

【目的】明确嘧菌酯对4种病原真菌的活性及旁路氧化酶抑制剂水杨肟酸(SHAM)的协同增效作用,探讨嘧菌酯抑制菌丝呼吸的作用机理及旁路氧化的作用。【方法】测定嘧菌酯单独使用或和SHAM协同使用对病原真菌菌丝生长和孢子萌发的抑制及对其它生物学性状的影响。利用氧电极溶氧仪测定嘧菌酯及SHAM对4种病原真菌菌丝呼吸耗氧的影响。【结果】嘧菌酯对辣椒炭疽病菌(辣椒炭疽)、黄瓜灰霉病菌、水稻纹枯病菌、稻瘟病菌的菌丝生长,对辣椒炭疽病菌、黄瓜灰霉病菌和稻瘟病菌的孢子萌发、孢子产生,对水稻纹枯病菌的菌核生成有抑制作用以及对辣椒炭疽病菌和稻瘟病菌的黑色素形成稍有延缓作用。SHAM对嘧菌酯毒力有显著的增效作用。菌丝耗氧率测定表明嘧菌酯在作用的初始阶段对4种病原真菌的菌丝呼吸均有抑制,抑制作用随药剂浓度提高而增强。随处理时间延长,菌丝恢复呼吸且呼吸作用的恢复不受SHAM抑制。【结论】延长处理时间情况下嘧菌酯丧失对菌丝呼吸耗氧的抑制作用,不是旁路氧化作用引起的,而是存在其它机制。

[Objective] The study was conducted to make clear the activity of azoxystrobin to four plant pathogens and the synergistic effects of salicylhydroxamic acid （SHAM） which acted on the alternative oxidase. It was also conducted to be aware of the mechanism of azoxystrobin on mycelial respiration and the influence of SHAM. [ Method ] The activity test of azoxystrobin and SHAM was carried out with a mycelial linear growth test and spore germination test. Other related biological properties were observed. Inhibition of azoxystrobin and SHAM on four pathogens was determined with an SP-Ⅱoxygraph system. [ Result] Azoxystrobin inhibited mycelial growth in Colletotrichum capsici, Botrytis cinerea, Rhizoctonia solani and Magnaporthe grisea respectively. It also inhibited conidia germination, conidia production in Colletotrichum capsici, Botrytis cinerea Magnaporthe grisea and sclerotia formation in Rhizoctonia solani. Moreover, it created stayed pigment biosynthesis in Colletotrichum capsici and Magnaporthe grisea. SHAM enhanced inhibition by azoxystrobin. An oxygen consumption test of the mycelia showed that azoxystrobin inhibited all four fungi＇s respiration in the early stages. With the concentration rising up, the effectiveness increased. However, as time went on, the respiration of the mycelia treated with fungicides recovered and SHAM could not inhibit oxygen consumption. [ Conclusion ] This reaction between the mycelia and the fungicides appeared not to initiate alternative respiration but rather the other mechanism created a lack of efficacy.