銅及其與四環素的聯合暴露對斑馬魚胚胎的毒性效應

近年來工業和養殖業中銅和四環素的濫用，導致了一定程度的水環境污染問題。為探究銅與四環素對水生生物的毒害作用，選擇斑馬魚作為受試生物，研究了銅及其與四環素的聯合暴露對斑馬魚胚胎的毒性效應，並進一步探索了其中可能的致毒機制。結果表明：銅在低濃度下(10%致死濃度LC₁₀=2.5μg·L⁻¹,10%效應濃度EC₁₀=0.1μg·L⁻¹)明顯延遲了斑馬魚胚胎的孵化、卵黃囊吸收、頭部、魚鰾和體長等生長指標的發育，同時在心臟區域引起了明顯的細胞凋亡效應。幼魚體內總銅含量檢測結果顯示低濃度下銅的生物利用度相對更高。基因表達結果顯示環境濃度的銅可能通過影響神經和心臟相關基因的表達引起斑馬魚胚胎的神經發育和心臟發育異常。銅和四環素的聯合暴露實驗結果表明二者的複合污染類型為拮抗作用，且兩者相互作用可以形成絡合物。綜合以上結論，說明環境濃度的銅可能通過細胞凋亡、分子水準的變化等方式對水生生物的早期生長發育產生危害，如延遲生長發育、神經及心臟發育異常，另外銅可通過和四環素等環境中其他污染物的結合改變銅的生物有效性和毒性。
With the increase use of copper and tetracycline in industry and agriculture, their aquatic environmental concentration increased greatly in recent years. This study aims to examine the developmental toxicity of Cu and tetracycline on zebrafish embryos (Danio rerio) and further explore its molecular mechanism. Cu shows high toxicity to zebrafish embryos (LC₁₀=2.5 μg·L⁻¹, EC₁₀=0.1 μg·L⁻¹), retarding the development and inducing apoptosis in the heart area of zebrafish larvae. The in vivo uptake of total Cu (96 h) in exposed embryos suggests that the uptake rate is relatively higher in low concentrations as compared to that of high concentrations. Gene expression study results showed that exposure to Cu upregulated gene expression level of Nkx2.5, which is responsible to cardiac development in zebrafish larvae. Exposure to Cu affected the gene expression level of several neuron development governing genes selected in this study. The results obtained in the co-exposure to Cu and tetracycline suggest that the combined toxicity is antagonism. This study suggests that exposure to Cu inhibits embryonic growth, induces the developmental anomaly of the nervous and heart in zebrafish embryos at environmental relevant concentrations. Co-exposure of Cu with other environmental contaminants such as tetracycline can change the bioavailability and the associated toxicity of Cu in aquatic organisms. Copyright © 2015 中國科學院生態環境研究中心.