Irish Centre for Environmental Toxicology, Galway-Mayo Institute of Technology, Galway, Ireland.
Chemosphere. 2011 Jul;84(5):657-63. doi: 10.1016/j.chemosphere.2011.03.033. Epub 2011 Apr 13.
Pharmaceuticals, including the lipid regulator gemfibrozil and the non-steroidal anti-inflammatory drug diclofenac have been identified in waste water treatment plant effluents and receiving waters throughout the western world. The acute and chronic toxicity of these compounds was assessed for three freshwater species (Daphnia magna, Pseudokirchneriella subcapitata, Lemna minor) using standardised toxicity tests with toxicity found in the non-environmentally relevant mid mg L(-1) concentration range. For the acute endpoints (IC(50) and EC(50)) gemfibrozil showed higher toxicity ranging from 29 to 59 mg L(-1) (diclofenac 47-67 mg L(-1)), while diclofenac was more toxic for the chronic D. magna 21 d endpoints ranging from 10 to 56 mg L(-1) (gemfibrozil 32-100 mg L(-1)). These results were compared with the expression of several biomarkers in the zebra mussel (Dreissena polymorpha) 24 and 96 h after exposure by injection to concentrations of 21 and 21,000 μg L(-1) corresponding to nominal concentrations of 1 and 1000 μg L(-1). Exposure to gemfibrozil and diclofenac at both concentrations significantly increased the level of lipid peroxidation, a biomarker of damage. At the elevated nominal concentration of 1000 μg L(-1) the biomarkers of defence glutathione transferase and metallothionein were significantly elevated for gemfibrozil and diclofenac respectively, as was DNA damage after 96 h exposure to gemfibrozil. No evidence of endocrine disruption was observed using the alkali-labile phosphate technique. Results from this suite of biomarkers indicate these compounds can cause significant stress at environmentally relevant concentrations acting primarily through oxidation pathways with significant destabilization of the lysosomal membrane and that biomarker expression is a more sensitive endpoint than standardised toxicity tests.
药品，包括脂调节剂吉非贝齐和非甾体抗炎药双氯芬酸，已在世界各地的废水处理厂废水和受纳水中被发现。使用标准化毒性试验，对三种淡水物种（大型溞、斜生栅藻、浮萍）评估了这些化合物的急性和慢性毒性，毒性发现于非环境相关的中 mg/L(-1)浓度范围内。对于急性终点（IC(50)和 EC(50)），吉非贝齐表现出较高的毒性，范围从 29 到 59 mg/L(-1)（双氯芬酸 47-67 mg/L(-1)），而双氯芬酸对慢性大型溞 21 d 终点更具毒性，范围从 10 到 56 mg/L(-1)（吉非贝齐 32-100 mg/L(-1)）。这些结果与斑马贻贝（Dreissena polymorpha）暴露于 21 和 21000 μg/L(-1)浓度（相当于名义浓度 1 和 1000 μg/L(-1)）24 和 96 h 后几种生物标志物的表达进行了比较。暴露于吉非贝齐和双氯芬酸在两个浓度下均显著增加了脂质过氧化水平，这是一种损伤的生物标志物。在名义浓度为 1000 μg/L(-1)时，吉非贝齐和双氯芬酸的防御性谷胱甘肽转移酶和金属硫蛋白的生物标志物分别显著升高，暴露于吉非贝齐 96 h 后 DNA 损伤也显著升高。使用碱性不稳定磷酸盐技术未观察到内分泌干扰的证据。这组生物标志物的结果表明，这些化合物在环境相关浓度下可引起显著的应激，主要通过氧化途径作用，显著破坏溶酶体膜的稳定性，并且生物标志物表达比标准化毒性试验更敏感。
