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咯菌腈敏感和抗性灰葡萄孢菌分离株中乙烯菌核利引起的脂质过氧化和膜破坏

Lipid Peroxidation and Membrane Disruption by Vinclozolin in Dicarboximide-Susceptible and -Resistant Isolates of Botrytis cinerea.

作者信息

Choi GJ, Lee HJ, Cho KY

机构信息

Korea Research Institute of Chemical Technology, Jang-dong 100, Taejon, 305-606, Korea

出版信息

Pestic Biochem Physiol. 1996 May;55(1):29-39. doi: 10.1006/pest.1996.0032.

DOI:10.1006/pest.1996.0032
PMID:8980027
Abstract

A dicarboximide-susceptible (DS) isolate and a dicarboximide-resistant (DR) isolate of Botrytis cinerea were compared with regard to spore germination, mycelial growth, cellular leakage, and lipid peroxidation upon treatment with the dicarboximide fungicide vinclozolin. The fungicide inhibited spore germination and mycelial growth of the DS isolate, but not those of the DR isolate. The inhibitory effect of the fungicide was greater on mycelial growth than on spore germination of the DS isolate. Significant cellular leakage from the fungicide-treated DS or DR isolate began to increase after 24 hr incubation, depending on the concentration of the fungicide and the duration of incubation time. However, the magnitude of cellular leakage was much greater from the DS isolate than from the DR isolate. Vinclozolin caused considerable lipid peroxidation in the DS isolate, whereas little or no lipid peroxidation occurred in the DR isolate treated with the fungicide. Lipid peroxidation preceded cellular leakage from the DS isolate following fungicide treatment. The effects of the fungicide on mycelial growth, cellular leakage, and lipid peroxidation of the DS isolate were all reversed by the addition of alpha-tocopherol to the incubation medium. These results demonstrate that vinclozolin causes significant lipid peroxidation and subsequent cellular leakage from a DS isolate, but not from a DR isolate. Furthermore, they suggest that the mechanism of action of dicarboximide fungicides is associated with membrane lipid peroxidation.

摘要

就用二甲酰亚胺类杀菌剂乙烯菌核利处理后的孢子萌发、菌丝生长、细胞渗漏和脂质过氧化情况,对灰葡萄孢的一个二甲酰亚胺敏感(DS)分离株和一个二甲酰亚胺抗性(DR)分离株进行了比较。该杀菌剂抑制了DS分离株的孢子萌发和菌丝生长,但对DR分离株没有抑制作用。该杀菌剂对DS分离株菌丝生长的抑制作用比对孢子萌发的抑制作用更大。用杀菌剂处理后的DS或DR分离株,在孵育24小时后,显著的细胞渗漏开始增加,这取决于杀菌剂的浓度和孵育时间的长短。然而,DS分离株的细胞渗漏程度比DR分离株大得多。乙烯菌核利在DS分离株中引起了相当程度的脂质过氧化,而在用该杀菌剂处理的DR分离株中几乎没有或没有脂质过氧化发生。在杀菌剂处理后,DS分离株的脂质过氧化先于细胞渗漏出现。向孵育培养基中添加α-生育酚后,该杀菌剂对DS分离株的菌丝生长、细胞渗漏和脂质过氧化的影响均被逆转。这些结果表明,乙烯菌核利会导致DS分离株发生显著的脂质过氧化并随后出现细胞渗漏,但不会导致DR分离株出现这种情况。此外,这些结果表明二甲酰亚胺类杀菌剂的作用机制与膜脂质过氧化有关。

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