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脂肪动激素诱导大猿叶虫血淋巴抗氧化能力增强以应对氧化应激。

Adipokinetic hormone-induced enhancement of antioxidant capacity of Pyrrhocoris apterus hemolymph in response to oxidative stress.

作者信息

Vecera Josef, Krishnan Natraj, Alquicer Glenda, Kodrík Dalibor, Socha Radomír

机构信息

Institute of Entomology, Academy of Sciences, Branisovská 31, CZ-370 05 Ceské Budejovice, Czech Republic.

出版信息

Comp Biochem Physiol C Toxicol Pharmacol. 2007 Sep;146(3):336-42. doi: 10.1016/j.cbpc.2007.04.005. Epub 2007 Apr 19.

DOI:10.1016/j.cbpc.2007.04.005
PMID:17512258
Abstract

The in vivo effects of oxidative stress on adipokinetic hormone (AKH) titer in short-winged (brachypterous) males of the firebug Pyrrhocoris apterus were tested using paraquat (PQ), a bipyridilium herbicide. PQ undergoes a cyclic redox reaction with oxygen during microsomal and electron transfer reactions forming free radicals in the insect body. Oxidative insult (40 pmol PQ) resulted in enhanced protein carbonylation (a biomarker for oxidative stress) and a depletion of glutathione (GSH) pool in the hemolymph. Interestingly, AKH titer was significantly enhanced in hemolymph at 4 h post inoculation of PQ, while its content in CNS (brain with corpora cardiaca) showed non-specific changes in comparable period. Co-injection of AKH with PQ (40 pmol each) reversed these effects by decreasing protein carbonyl formation, increasing reduced GSH levels, and enhancing the total antioxidant capacity of cell free plasma. Our results indicate that there is a positive feedback regulation between an oxidative stressor action and the level of AKH in insect body, and that AKHs might be involved in the activation of antioxidant protection mechanism.

摘要

使用百草枯(PQ,一种联吡啶类除草剂)测试了氧化应激对萤火虫 Pyrrhocoris apterus 短翅(残翅)雄性体内脂肪动激素(AKH)滴度的影响。PQ 在微粒体和电子转移反应过程中与氧气发生循环氧化还原反应,在昆虫体内形成自由基。氧化损伤(40 pmol PQ)导致血淋巴中蛋白质羰基化增强(氧化应激的生物标志物)以及谷胱甘肽(GSH)池耗竭。有趣的是,在接种 PQ 后 4 小时,血淋巴中 AKH 滴度显著增强,而在同一时期其在中枢神经系统(脑和心侧体)中的含量显示出非特异性变化。将 AKH 与 PQ(各 40 pmol)共同注射可通过减少蛋白质羰基形成、增加还原型 GSH 水平以及提高无细胞血浆的总抗氧化能力来逆转这些影响。我们的结果表明,在昆虫体内氧化应激源作用与 AKH 水平之间存在正反馈调节,并且 AKHs 可能参与抗氧化保护机制的激活。

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