水杨基羟肟酸的毒性及其对嘧菌酯和吡菌酯敏感性的影响。

Jiehui Song, Zhiying Wang, Sijie Zhang, Yan Wang, You Liang, Qigen Dai, Zhongyang Huo, Ke Xu
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引用次数: 1

摘要

水稻假黑穗病是水稻最严重的病害之一。以杀菌剂为主的化学防治是防治RFS的重要措施。在体外对醌外抑制剂(QoI)的敏感性测定中,为了抑制植物病原真菌的选择性氧化酶,通常在人工培养基中添加水杨酸羟肟酸(SHAM)。然而,一些研究表明,由于其毒性,人工培养基不应包括SHAM。是否应该在细菌对qi杀菌剂的敏感性测定中加入SHAM仍是未知的。本研究选用马铃薯蔗糖琼脂(PSA)和最小培养基(MM)两种培养基,分别检测了假体菌对偶氮嘧菌酯和吡咯菌酯的SHAM毒性和敏感性。假药可显著抑制葡萄球菌菌丝生长、分生孢子萌发、过氧化物酶(POD)和酯酶活性。在PSA和MM上,SHAM抑制10种真菌菌丝生长50% (EC50)的平均有效浓度分别为27.41和12.75 μg/mL。SHAM对菌株HWD和JS60孢子萌发的EC50值分别为70.36和44.69 μg/mL。30 μg/mL的SHAM显著抑制HWD和JS60分离株的POD和酯酶活性,10 μg/mL的SHAM也显著抑制HWD分离株的POD活性。此外,虚假的显著降低azoxystrobin EC50值和EC90值和pyraclostrobin PSA和毫米。即使在虚假的存在10μg / mL,平均的EC50值十对隔离对PSA azoxystrobin下降1.7倍和4.8倍毫米,和pyraclostrobin在PSA下降了2.8倍和4.8倍。因此,这些结果表明,假不应包含在人工媒体对测定的灵敏度QoI杀菌剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Toxicity of Salicylhydroxamic Acid and Its Effect on the Sensitivity of <i>Ustilaginoidea virens</i> to Azoxystrobin and Pyraclostrobin.

The Toxicity of Salicylhydroxamic Acid and Its Effect on the Sensitivity of <i>Ustilaginoidea virens</i> to Azoxystrobin and Pyraclostrobin.

The Toxicity of Salicylhydroxamic Acid and Its Effect on the Sensitivity of <i>Ustilaginoidea virens</i> to Azoxystrobin and Pyraclostrobin.

The Toxicity of Salicylhydroxamic Acid and Its Effect on the Sensitivity of Ustilaginoidea virens to Azoxystrobin and Pyraclostrobin.

Rice false smut (RFS) caused by Ustilaginoidea virens has been one of the most severe rice diseases. Fungicide-based chemical control is a significant measure to control RFS. In the sensitivity determination of quinone outside inhibitor (QoI) fungicide in vitro, salicylhydroxamic acid (SHAM) has been commonly added to artificial culture media in order to inhibit alternative oxidase of phytopathogenic fungi. However, some studies showed that artificial media should not include SHAM due to its toxicity. Whether SHAM should be added in the assay of U. virens sensitivity to QoI fungicide remains unknown. In this study, two appropriate media, potato sucrose agar (PSA) and minimal medium (MM), were selected to test SHAM toxicity and sensitivity of U. virens to azoxystrobin and pyraclostrobin. The mycelial growth and sensitivity to azoxystrobin and pyraclostrobin had no significant difference between on PSA and MM. SHAM could significantly inhibit mycelial growth, conidial germination, peroxidase (POD) and esterase activity of U. virens. Average effective concentration for inhibiting 50% (EC50) values of SHAM against mycelial growth of ten U. virens were 27.41 and 12.75 μg/mL on PSA and MM, respectively. The EC50 values of SHAM against conidial germination of isolates HWD and JS60 were 70.36 and 44.69 μg/mL, respectively. SHAM at 30 μg/mL significantly inhibited POD and esterase activity of isolates HWD and JS60, and even SHAM at 10 μg/mL significantly inhibited POD activity of isolate HWD. In addition, SHAM significantly reduced EC50 values and EC90 values of azoxystrobin and pyraclostrobin on both PSA and MM. Even in the presence of SHAM at 10 μg/mL, average EC50 values of ten U. virens isolates for azoxystrobin decreased 1.7-fold on PSA and 4.8-fold on MM, and for pyraclostrobin that decreased 2.8-fold on PSA and 4.8-fold on MM. Therefore, these results suggest that SHAM should not be included in artificial media in the assay of U. virens sensitivity to QoI fungicides.

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