Li-Byarlay Hongmei, Huang Ming Hua, Simone-Finstrom Michael, Strand Micheline K, Tarpy David R, Rueppell Olav
Department of Entomology, North Carolina State University, Raleigh, NC, USA; W.M. Keck Center for Behavioral Biology, North Carolina State University, Raleigh, NC, USA; Department of Biology, University of North Carolina at Greensboro, Greensboro, NC, USA.
Eurofins Agroscience Services, Prospect Hill, NC, USA.
Exp Gerontol. 2016 Oct;83:15-21. doi: 10.1016/j.exger.2016.07.003. Epub 2016 Jul 12.
Oxidative stress can lead to premature aging symptoms and cause acute mortality at higher doses in a range of organisms. Oxidative stress resistance and longevity are mechanistically and phenotypically linked; considerable variation in oxidative stress resistance exists among and within species and typically covaries with life expectancy. However, it is unclear whether stress-resistant, long-lived individuals avoid, repair, or tolerate molecular damage to survive longer than others. The honey bee (Apis mellifera L.) is an emerging model system that is well-suited to address this question. Furthermore, this species is the most economically important pollinator, whose health may be compromised by pesticide exposure, including oxidative stressors. Here, we develop a protocol for inducing oxidative stress in honey bee males (drones) via Paraquat injection. After injection, individuals from different colony sources were kept in common social conditions to monitor their survival compared to saline-injected controls. Oxidative stress was measured in susceptible and resistant individuals. Paraquat drastically reduced survival but individuals varied in their resistance to treatment within and among colony sources. Longer-lived individuals exhibited higher levels of lipid peroxidation than individuals dying early. In contrast, the level of protein carbonylation was not significantly different between the two groups. This first study of oxidative stress in male honey bees suggests that survival of an acute oxidative stressor is due to tolerance, not prevention or repair, of oxidative damage to lipids. It also demonstrates colony differences in oxidative stress resistance that might be useful for breeding stress-resistant honey bees.
氧化应激可导致一系列生物体出现早衰症状，并在高剂量时导致急性死亡。氧化应激抗性与寿命在机制和表型上存在关联；物种之间和物种内部的氧化应激抗性存在相当大的差异，并且通常与预期寿命相关。然而，尚不清楚抗应激、长寿的个体是通过避免、修复还是耐受分子损伤来比其他个体存活更长时间。蜜蜂（西方蜜蜂）是一个新兴的模型系统，非常适合解决这个问题。此外，该物种是经济上最重要的传粉者，其健康可能会因接触包括氧化应激源在内的农药而受到损害。在这里，我们开发了一种通过百草枯注射在雄蜂（雄蜂）中诱导氧化应激的方案。注射后，将来自不同蜂群来源的个体置于共同的社会条件下，与注射生理盐水的对照组相比，监测它们的存活情况。在易感和抗性个体中测量氧化应激。百草枯显著降低了存活率，但个体在蜂群来源内部和之间对处理的抗性存在差异。寿命较长的个体比早死的个体表现出更高水平的脂质过氧化。相比之下，两组之间的蛋白质羰基化水平没有显著差异。这项对雄蜂氧化应激的首次研究表明，急性氧化应激源的存活是由于对脂质氧化损伤的耐受，而不是预防或修复。它还证明了蜂群在氧化应激抗性方面的差异，这可能有助于培育抗应激的蜜蜂。
