人为的环境变化使野生动植物暴露于许多污染物中。其中,对流层臭氧是全球关注和高度有效的助氧化剂。此外,人类活动包括对野生动物的其他影响,例如,改变了城市中的食物供应和病原体分布。这些共同发生的栖息地变化可能相互作用,从而调节与人为变化相关的生理反应和成本。例如,许多与人类相关的食品(例如,野鸟的食物废物和饲养者)比ω3多不饱和脂肪酸(PUFA)含有相对更多的ω6。来自ω6-PUFA的代谢物可以增强炎症和氧化应激,而相反的反应与ω3衍生的代谢物有关。因此,我们假设ω6-和ω3-PUFA的不同摄入量调节鸟类的氧化应激状态,从而影响对促氧化剂的反应。为了测试这个,我们在使用圈养斑马雀(Taeniopygiaguttata)的全因子实验中操纵了饮食ω6:ω3的比例和臭氧水平。此外,我们模拟了一种感染,从而也触发免疫系统的适应性促氧化剂释放(即,氧化爆发),通过注射脂多糖。在正常空气条件下,与ω6饮食鸟类相比,ω3饮食鸟类的抗氧化剂比率(GSH/GSSG比率)较低。当暴露于臭氧时,然而,饮食效果消失了。相反,臭氧暴露总体上降低了关键抗氧化剂谷胱甘肽(tGSH)的总浓度。此外,与饲喂富含ω3饮食的鸟类相比,富含ω6饮食的鸟类具有更高的抗氧化能力(OXY)。有趣的是,只有免疫挑战增加了氧化损伤,表明免疫系统的氧化爆发超越了其他促氧化过程,包括饮食。一起来看,我们的结果表明,臭氧,膳食PUFA,感染都会影响氧化还原系统,但是以不同的方式,这表明潜在的反应是分离的,尽管它们都增加了促氧化剂的暴露或产生。尽管在独立的生物标志物中缺乏明显的累积效应,组合的单一效应可以一起降低暴露于病原体的野生鸟类的整体细胞功能和效率,臭氧,和人为食物来源。
Anthropogenic changes to the environment expose wildlife to many pollutants. Among these, tropospheric ozone is of global concern and a highly potent pro-oxidant. In addition, human activities include several other implications for wildlife, e.g., changed food availability and changed distribution of pathogens in cities. These co-occurring habitat changes may interact, thereby modulating the physiological responses and costs related to anthropogenic change. For instance, many food items associated with humans (e.g., food waste and feeders for wild birds) contain relatively more ω6-than ω3-polyunsaturated fatty acids (PUFAs). Metabolites derived from ω6-PUFAs can enhance inflammation and oxidative stress towards a stimulus, whereas the opposite response is linked to ω3-derived metabolites. Hence, we hypothesized that differential intake of ω6-and ω3-PUFAs modulates the oxidative stress state of birds and thereby affects the responses towards pro-oxidants. To test this, we manipulated dietary ω6:ω3 ratios and ozone levels in a full-factorial experiment using captive zebra finches (Taeniopygia guttata). Additionally, we simulated an infection, thereby also triggering the immune system\'s adaptive pro-oxidant release (i.e., oxidative burst), by injecting lipopolysaccharide. Under normal air conditions, the ω3-diet birds had a lower antioxidant ratio (GSH/GSSG ratio) compared to the ω6-diet birds. When exposed to ozone, however, the diet effect disappeared. Instead, ozone exposure overall reduced the total concentration of the key antioxidant glutathione (tGSH). Moreover, the birds on the ω6-rich diet had an overall higher antioxidant capacity (OXY) compared to birds fed a ω3-rich diet. Interestingly, only the immune challenge increased oxidative damage, suggesting the oxidative burst of the immune system overrides the other pro-oxidative processes, including diet. Taken together, our results show that ozone, dietary PUFAs, and infection all affect the redox-system, but in different ways, suggesting that the underlying responses are decoupled despite that they all increase pro-oxidant exposure or generation. Despite lack of apparent cumulative effect in the independent biomarkers, the combined single effects could together reduce overall cellular functioning and efficiency over time in wild birds exposed to pathogens, ozone, and anthropogenic food sources.