Faculty of Natural Resources Management, Lakehead University, Thunder Bay, ON, Canada P7B 5E1.
Aquatic Contaminants Research Division, Environment Canada, Burlington, ON, Canada L7R 4A6.
Aquat Toxicol. 2014 Sep;154:253-69. doi: 10.1016/j.aquatox.2014.05.026. Epub 2014 Jun 2.
Mixtures of metals and polycyclic aromatic hydrocarbons (PAHs) occur ubiquitously in aquatic environments, yet relatively little is known regarding their combined toxicities. Emerging reports investigating the additive mortality in metal-PAH mixtures have indicated that more-than-additive effects are equally as common as strictly-additive effects, raising concern for ecological risk assessment typically based on the summation of individual toxicities. Moreover, the current separation of focus between in vivo and in vitro studies, and fine- and coarse-scale endpoints, creates uncertainty regarding the mechanisms of co-toxicity involved in more-than-additive effects on whole organisms. Drawing from literature on metal and PAH toxicity in bacteria, protozoa, invertebrates, fish, and mammalian models, this review outlines several key mechanistic interactions likely to promote more-than-additive toxicity in metal-PAH mixtures. Namely, the deleterious effects of PAHs on membrane integrity and permeability to metals, the potential for metal-PAH complexation, the inhibitory nature of metals to the detoxification of PAHs via the cytochrome P450 pathway, the inhibitory nature of PAHs towards the detoxification of metals via metallothionein, and the potentiated production of reactive oxygenated species (ROS) in certain metal (e.g. Cu) and PAH (e.g., phenanthrenequinone) mixtures. Moreover, the mutual inhibition of detoxification suggests the possibility of positive feedback among these mechanisms. The individual toxicities and interactive aspects of contaminant transport, detoxification, and the production of ROS are herein discussed.
金属和多环芳烃（PAHs）混合物普遍存在于水生环境中，但对于它们的联合毒性知之甚少。新兴的关于金属-PAH 混合物的附加死亡率的报告表明，超相加效应与严格相加效应同样常见，这引起了人们对通常基于个体毒性总和的生态风险评估的关注。此外，目前在体内和体外研究以及精细和粗糙尺度终点之间的焦点分离，导致对整个生物体中涉及超相加效应的共同毒性的机制存在不确定性。本综述借鉴了关于金属和 PAH 在细菌、原生动物、无脊椎动物、鱼类和哺乳动物模型中的毒性的文献，概述了几种可能促进金属-PAH 混合物中超相加毒性的关键机制相互作用。即，PAHs 对膜完整性和金属通透性的有害影响、金属-PAH 络合的可能性、金属通过细胞色素 P450 途径对 PAH 解毒的抑制作用、PAHs 对金属解毒的抑制作用通过金属硫蛋白，以及某些金属（例如铜）和 PAH（例如菲醌）混合物中活性氧物质（ROS）的增强产生。此外，解毒的相互抑制表明这些机制之间存在正反馈的可能性。本文讨论了污染物运输、解毒和 ROS 产生的个体毒性和相互作用方面。
