State Key Laboratory of Marine Environmental Science, Xiamen University, No. 182 Daxue Road, Siming District, Xiamen 361005, China.
Mar Pollut Bull. 2012 Jul;64(7):1445-51. doi: 10.1016/j.marpolbul.2012.04.007. Epub 2012 May 23.
The mode of action of PAHs that causes fish developmental malformations is unclear. The embryotoxicity of marine medaka (Oryzias melastigma) was investigated after individual exposure to three- to five-ring PAHs Phe, Py, and BaP or co-exposure with α-ANF for 18 days. We found that the relationships between EROD induction and developmental deformities of embryos showed a various pattern under different exposure scenarios of Phe, Py, and BaP, which suggested possibly different modes of action in determining the developmental toxicities. As for co-exposure scenarios of each PAH combined with ANF, it showed potentially synergistic effects. The inhibited CYP1A mediated enzyme activity by ANF after co-exposure did not effectively alleviate developmental toxicity of embryo. It showed potentially synergistic effects after co-exposure of marine fish embryos to CYP1A inhibitors and PAH-type CYP1A inducers. Heart deformities in the early life stages of marine medaka were recommended as a biomarker for indicating the extent of PAH pollution.
多环芳烃导致鱼类发育畸形的作用模式尚不清楚。本研究采用海洋型原尾鱼（Oryzias melastigma）为实验动物，在个体暴露于三种至五种环多环芳烃（菲、芘和 BaP）或与 α-ANF 共同暴露 18 天后，检测了其胚胎毒性。我们发现，在不同的菲、芘和 BaP 暴露情况下，EROD 诱导与胚胎发育畸形之间的关系呈现出不同的模式，这表明在确定发育毒性方面可能存在不同的作用模式。对于每种 PAH 与 ANF 联合暴露的情况，均表现出潜在的协同作用。经共同暴露后，ANF 抑制 CYP1A 介导的酶活性并不能有效缓解胚胎的发育毒性。海洋鱼类胚胎同时暴露于 CYP1A 抑制剂和 PAH 型 CYP1A 诱导剂时，表现出潜在的协同作用。海洋型原尾鱼早期心脏畸形可作为指示多环芳烃污染程度的生物标志物。
