Municipal wastewater effluent is a major source of aquatic pollution and has potential to impact cellular energy metabolism. However, it is poorly understood whether wastewater exposure impacts whole-animal metabolism and whether this can be accommodated with adjustments in respiratory physiology. We caged bluegill sunfish (Lepomis macrochirus) for 21 days at two sites downstream (either 50 or 830 m) from a wastewater treatment plant (WWTP). Survival was reduced in fish caged at both downstream sites compared to an uncontaminated reference site. Standard rates of O₂ consumption increased in fish at contaminated sites, reflecting a metabolic cost of wastewater exposure. Several physiological adjustments accompanied this metabolic cost, including an expansion of the gill surface area available for gas exchange (reduced interlamellar cell mass), a decreased blood-O₂ affinity (which likely facilitates O₂ unloading at respiring tissues), increased respiratory capacities for oxidative phosphorylation in isolated liver mitochondria (supported by increased succinate dehydrogenase, but not citrate synthase, activity), and decreased mitochondrial emission of reactive oxygen species (ROS). We conclude that exposure to wastewater effluent invokes a metabolic cost that leads to compensatory respiratory improvements in O₂ uptake, delivery, and utilization.

中文翻译：

---

暴露于废水中的代谢成本导致蓝g翻车鱼的呼吸生理发生补偿性调整。

市政废水是水污染的主要来源，具有影响细胞能量代谢的潜力。但是，人们对废水的暴露是否会影响整个动物的新陈代谢以及是否可以通过调整呼吸生理来适应这一点知之甚少。我们将蓝g翻车鱼（Lepomis macrochirus）放在废水处理厂（WWTP）下游的两个位置（50或830 m）的网箱中21天。与未污染的参考地点相比，在两个下游地点关在笼中的鱼的存活率降低了。O _2的标准量受污染地点鱼的消费量增加，反映出废水暴露的代谢成本。伴随着这种代谢成本的几项生理调节包括：扩大可用于气体交换的ill表面积（减少层间细胞质量），降低血液对O _2的亲和力（可能促进呼吸组织中O _2的卸荷），增加呼吸能力。分离的肝线粒体中的氧化磷酸化（由琥珀酸脱氢酶的增加，但柠檬酸合酶的活性支持）和活性氧（ROS）的线粒体释放减少。我们得出的结论是，暴露于废水中会引起代谢成本，从而导致O _2的代偿性呼吸改善。 吸收，传递和利用。