Neonicotinoids, the most widely used systemic insecticides in the world, have been shown to be one of the risk factors to colony collapse disorder (CCD). Although the exact underlying mechanisms of honeybee (Apis mellifera) CCD have not yet been confirmed, we postulated that mitochondrial DNA (mtDNA) damage in honeybees resulting from sublethal neonicointoids exposure could be a plausible cause leading to malfunctioning thermoregulation. In this study, we used the relative mitochondrial DNA copy number (RmtDNAcn) as an early biomarker to elucidate the association between chronic sub-lethal neonicotinoids exposure and mtDNA damage in honeybees. We collected adult worker bees from hives that were either served as controls or exposed to a sub-lethal level of imidacloprid or clothianidin in three different brood generations that coincided with before, during, and after neonicotinoids treatments. Although there were no apparent adverse health effects in individual bees or the whole colony during and after neonicotinoids administration, the cumulative mtDNA damage in winter bees might have negatively impacted their hives’ survival over winter due to the perturbation of energy metabolism. These results contribute to the explanation of a potential mechanism of CCD.

中文翻译：

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线粒体功能障碍：蜜蜂菌落崩溃症（CCD）的合理途径

新烟碱类化合物是世界上使用最广泛的系统性杀虫剂，已被证明是导致菌落衰竭（CCD）的危险因素之一。尽管蜜蜂的确切内在机制（意大利蜜蜂）CCD尚未得到证实，我们推测亚致死性新烟碱类药物暴露导致蜜蜂的线粒体DNA（mtDNA）损伤可能是导致温度调节异常的合理原因。在这项研究中，我们使用相对线粒体DNA拷贝数（RmtDNAcn）作为早期生物标志物，阐明了慢性亚致死性新烟碱暴露与蜜蜂中mtDNA损伤之间的关联。我们从蜂巢中收集了成年工蜂，这些蜂被用作对照，或者在新烟碱类药物治疗之前，期间和之后三种不同的育雏时期暴露于亚致死浓度的吡虫啉或可比丁。尽管在服用新烟碱类药物期间和之后对单个蜜蜂或整个菌落没有明显的不利健康影响，由于能量代谢的扰动，冬季蜜蜂中累积的mtDNA损伤可能对其蜂巢的冬季生存造成负面影响。这些结果有助于解释CCD的潜在机理。