Abstract：
Cadmium (Cd) is a toxic non-essential metal element that can enter the honey bee body through air, water and soil. Currently, there is a lack of sufficient research on the effects of Cd on A. cerana cerana, especially the potential risks of long-term exposure to sublethal concentrations. In order to ascertain the toxicological effects of the heavy metal Cd on bees, we performed laboratory-based toxicity experiments on worker bees and conducted analyses from three distinctive facets: antioxidative, immunological, and gut microbiota. The results showed that exposure of bees to high concentrations of Cd resulted in acute mortality, and the increase in mortality was concentration dependent. In long-term exposure to sublethal concentrations, Cd reduced the number of transcripts of antioxidant genes (AccSOD1, AccTPx3 and AccTPx4) and superoxide dismutase activity, causing an increase in malondialdehyde content. Simultaneously, the transcription of immune-related genes (AccAbaecin and AccApidaecin) and acetylcholinesterase activities was inhibited. Furthermore, Cd changes the structural characteristics of bacterial and fungal communities in the gut, disrupting the balance of microbial communities. In conclusion, the health and survival of honey bees are affected by Cd. This study provides a scientific basis for investigating the toxicological mechanisms and control strategies of the heavy metal Cd on honey bees, while facilitating a better understanding and protection of these valuable honey bees.
摘要：
镉（Cd）是一种有毒的非必需金属元素，可以通过空气进入蜜蜂体内，水和土壤。目前,对Cd对cerana的影响缺乏足够的研究，特别是长期暴露于亚致死浓度的潜在风险。为了确定重金属Cd对蜜蜂的毒理学效应，我们对工蜂进行了基于实验室的毒性实验，并从三个不同的方面进行了分析：抗氧化，免疫学，和肠道微生物群。结果表明，蜜蜂暴露于高浓度的Cd会导致急性死亡，死亡率的增加是浓度依赖性的。长期暴露于亚致死浓度,Cd降低了抗氧化基因（AccSOD1，AccTPx3和AccTPx4）的转录本数量和超氧化物歧化酶活性，导致丙二醛含量增加。同时,免疫相关基因(AccAbaecin和AccApidaecin)的转录和乙酰胆碱酯酶活性被抑制。此外，Cd改变了肠道细菌和真菌群落的结构特征,破坏微生物群落的平衡。总之,Cd影响蜜蜂的健康和生存。本研究为研究重金属Cd对蜜蜂的毒理机制和控制策略提供了科学依据。同时促进更好地理解和保护这些珍贵的蜜蜂。
