Nareshkumar Bharat, Akbar Shaik Mohammad, Sharma Hari Chand, Jayalakshmi Senigala K, Sreeramulu Kuruba
Department of Biochemistry, Gulbarga University, Gulbarga, Karnataka, India.
Entomology, International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), Patancheru, Telangana State, India.
Arch Insect Biochem Physiol. 2017 Sep;96(1). doi: 10.1002/arch.21401. Epub 2017 Jun 20.
Phthalic acid diamide insecticides are the most effective insecticides used against most of the lepidopteran pests including Helicoverpa armigera, a polyphagous pest posing threat to several crops worldwide. The present studies were undertaken to understand different target sites and their interaction with insect ryanodine receptors (RyR). Bioassays indicated that flubendiamide inhibited the larval growth in dose-dependent manner with LD value of 0.72 μM, and at 0.8 μM larval growth decreased by about 88%. Flubendiamide accelerated the Ca -ATPase activity in dose-dependent trend, and at 0.8 μM, the activity was increased by 77.47%. Flubendiamide impedes mitochondrial function by interfering with complex I and F F -ATPase activity, and at 0.8 μM the inhibition was found to be about 92% and 50%, respectively. In vitro incubation of larval mitochondria with flubendiamide induced the efflux of cytochrome c, indicating the mitochondrial toxicity of the insecticide. Flubendiamide inhibited lactate dehydrogenase and the accumulation of H O , thereby preventing the cells from lipid peroxidation compared to control larvae. At 0.8 μM the LDH, H O content and lipid peroxidation was inhibited by 98.44, 70.81, and 70.81%, respectively. Cytochrome P450, general esterases, AChE, and antioxidant enzymes (catalase and superoxide dismutase) exhibited a dose-dependent increasing trend, whereas alkaline phosphatase and the midgut proteases, except amino peptidase, exhibited dose-dependent inhibition in insecticide-fed larvae. The results suggest that flubendiamide induced the harmful effects on the growth and development of H. armigera larvae by inducing mitochondrial dysfunction and inhibition of midgut proteases, along with its interaction with RyR.
邻苯二甲酸二酰胺类杀虫剂是防治包括棉铃虫在内的大多数鳞翅目害虫最有效的杀虫剂，棉铃虫是一种多食性害虫，对全球多种作物构成威胁。本研究旨在了解不同的作用靶标位点及其与昆虫兰尼碱受体（RyR）的相互作用。生物测定表明，氟苯虫酰胺以剂量依赖的方式抑制幼虫生长，致死剂量（LD）值为0.72 μM，在0.8 μM时幼虫生长下降约88%。氟苯虫酰胺以剂量依赖的趋势加速Ca -ATP酶活性，在0.8 μM时，活性增加77.47%。氟苯虫酰胺通过干扰复合体I和F F -ATP酶活性来阻碍线粒体功能，在0.8 μM时，抑制率分别约为92%和50%。用氟苯虫酰胺对幼虫线粒体进行体外孵育可诱导细胞色素c外流，表明该杀虫剂具有线粒体毒性。与对照幼虫相比，氟苯虫酰胺抑制乳酸脱氢酶和H O 的积累，从而防止细胞发生脂质过氧化。在0.8 μM时，乳酸脱氢酶、H O 含量和脂质过氧化的抑制率分别为98.44%、70.81%和70.81%。细胞色素P450、一般酯酶、乙酰胆碱酯酶和抗氧化酶（过氧化氢酶和超氧化物歧化酶）呈现剂量依赖性增加趋势，而碱性磷酸酶和中肠蛋白酶（氨基肽酶除外）在喂食杀虫剂的幼虫中呈现剂量依赖性抑制。结果表明，氟苯虫酰胺通过诱导线粒体功能障碍和抑制中肠蛋白酶以及与RyR相互作用，对棉铃虫幼虫的生长发育产生有害影响。
