不同奈米鐵對青鱂魚早期發育階段之生物累積及毒性效應

Abstract

奈米零價鐵 (nanoscale zerovalent iron, nZVI) 具有高比表面積且強還原能力，故常被用於地下水或土壤汙染整治；此外，近年來研究指出nZVI會與氧氣作用而產生高反應性的活性氧物種 (reactive oxygen species, ROS)，可應用於廢水處理的高級氧化程序。然而一旦nZVI進入環境水體後，其在水域環境中的宿命及可能對環境生態或人類健康造成的影響目前仍不明確。本研究探討穩定化奈米零價鐵 (CMC-nZVI, 27.1±3.7 nm)、奈米氧化鐵 (nFe3O4, 30.1 ± 2.6 nm) 以及亞鐵離子(Fe2+) 對早期發育階段之青鱂魚的生物累積及毒性效應。三種鐵物種造成胚胎的死亡率依序為: CMC-nZVI > Fe2+ > nFe3O4。CMC-nZVI在較高濃度 ( > 100 mg/L)大量消耗暴露溶液中之溶氧，並經由氧化作用產生具毒性之Fe2+與ROS，胚胎的絨毛膜層受ROS及nZVI破壞使暴露溶液中nZVI及相關產物進入胚胎內而造成毒害效應。三種鐵物種處理在胚胎中均有生物累積的現象。此外，CMC-nZVI (暴露7日)對青鱂魚胚胎造成最嚴重之生長發育毒性，而nFe3O4及Fe2+對胚胎的影響程度則相對較低。三種鐵物種均會降低胚胎心跳速率並延遲其孵化；相較於nFe3O4及Fe2+，暴露於高濃度 (>100 mg/L) 的CMC-nZVI造成較嚴重之眼睛發育延遲及眼睛尺寸較小等現象。此外，暴露於三種鐵物種處理之孵化魚苗體內ROS含量相較於控制組均有提升的現象。其中，CMC-nZVI在低濃度 (25-50 mg/L) 即會顯著誘導魚苗體內ROS含量。nFe3O4及Fe2+提高SOD (superoxide dismutase) 活性，然而CMC-nZVI則是隨暴露劑量增加而顯著抑制SOD活性。CMC-nZVI於25 mg/L會誘導CAT (catalase, CAT) 活性，但CAT活性隨暴露劑量上升 (50-200 mg/L) 而下降；而在nFe3O4及Fe2+處理 (25-200 mg/L) 之孵化魚苗其CAT活性隨濃度增加而下降；僅有nFe3O4處理 (25-150 mg/L) 之孵化魚苗體內GR (glutathione reductase, GR) 活性上升。以三種鐵物種處理後之孵化魚苗組織切片結果並未觀察到有明顯的病理變化，但分別在腸道、腸壁、胰或身體組織中觀察到些微的鐵累積。綜合上述結果，相較於nFe3O4及Fe2+處理，CMC-nZVI對青鱂魚胚胎具有較高的急毒性及發育毒性，且三種處理均會對孵化之魚苗造成不同程度的氧化壓力。

Iron-based NPs have been used on wastewater treatment or environmental remediation applications. The public has raised concerns about the increased risk of exposure and toxicity to iron NPs for human and aquatic life. However, the fate and toxic effects of iron NPs in the aquatic ecosystem remain unclear at present. In this study, we have treated embryos of medaka (Oryzias latipes) fish with carboxymethyl cellulose stabilized nanoscale zero-valent iron (CMC-nZVI, 27.1±3.7 nm), nanoscale iron oxide (nFe3O4, 30.1±2.6 nm) and ferrous ion [Fe(II)aq] at dosages of 25-200 mg/L for a 7-day aqueous exposure. We have investigated the mortality, bioaccumulation potency, developmental toxicity and oxidative stress effects of two iron NPs and [Fe(II)aq] in early life stages of medaka. Results show CMC-nZVI caused the severest mortality and developmental toxic effects in embryos. The bioaccumulation potency in embryos exposed to all 3 iron species treatments (50-150 mg/L) was significantly higher than the control. Embryos treated with CMC-nZVI caused the greatest developmental toxicity including decrease in heart rate, eye size and hatching rate, thus leading to hatching delayed, and nFe3O4 while [Fe(II)aq] caused lesser and least effects. Also, intracellular levels of reactive oxygen species and activities of antioxidants such as superoxide dismutase and catalase were altered in hatchings from embryos treated with CMC-nZVI (>25 mg/L), nFe3O4 (200 mg/L) and [Fe(II)aq] (>50 mg/L). Based on histopathological analyses, all 3 iron species treatement didn’t cause pathological changes but led to a slight degree of iron accumulation in the alimentary canal, pancreas and body tissues. The results implicate a potential ecotoxicological impact of nZVI and related oxidized products on the aquatic environment.