van der Merwe Johannes A, Dubery Ian A
Department of Biochemistry, University of Johannesburg, Kingsway Campus, P.O. Box 524, Auckland Park 2006, South Africa.
J Plant Physiol. 2006 Jul;163(8):877-82. doi: 10.1016/j.jplph.2005.08.016. Epub 2005 Nov 9.
An inducer of acquired disease resistance in plants, benzo (1,2,3) thiadiazole-7-carbothioic acid S-methyl ester, exhibited direct, concentration-dependent inhibition of the NADH:ubiquinone oxidoreductase activity of complex I of the mitochondrial electron transport chain of cultured tobacco cells. The complex I activity was less sensitive to inhibition by salicylic acid, an endogenous activator of acquired disease resistance. Using a dichlorodihydrofluorescein assay, it was found that benzothiadiazole, salicylic acid and the complex I inhibitor rotenone, increased reactive oxygen species production within cells in a concentration-dependent manner. The results indicate that both benzothiadiazole and salicylic acid affect the mitochondria of treated plant cells and result in increased production of reactive oxygen species. The biochemical basis of this response could be related to the inhibition of the NADH:ubiquinone oxidoreductase activity of complex I that results in channelling of electrons via complex II, with concomitant higher levels of superoxide production.
植物后天抗病性的诱导剂苯并（1,2,3）噻二唑-7-硫代羧酸S-甲酯，对培养的烟草细胞线粒体电子传递链复合体I的NADH：泛醌氧化还原酶活性表现出直接的、浓度依赖性抑制。复合体I活性对后天抗病性的内源性激活剂水杨酸的抑制不太敏感。使用二氯二氢荧光素测定法发现，苯并噻二唑、水杨酸和复合体I抑制剂鱼藤酮以浓度依赖性方式增加细胞内活性氧的产生。结果表明，苯并噻二唑和水杨酸均影响处理过的植物细胞的线粒体，并导致活性氧产生增加。这种反应的生化基础可能与复合体I的NADH：泛醌氧化还原酶活性受到抑制有关，该抑制导致电子通过复合体II传导，同时超氧化物产生水平更高。
