| 摘要: | 近年來微/奈米塑膠被發現存在於自然環境、海洋生物體、食用的調味料（糖、鹽、蜂蜜）中，甚至是日常的塑膠茶包或奶瓶接觸熱水後都會釋放出塑膠微粒，人類透過攝食或呼吸不可避免的會暴露到塑膠微粒，因此對於塑膠微粒導致的健康影響議題受到關注。然而目前為止對微米塑膠的研究較多，而奈米塑膠的生物效應影響相關研究較缺乏。有限的證據顯示塑膠微粒可能於脂肪累積並影響脂肪的代謝，因此奈米塑膠可能作為環境因子，增進脂肪的形成及累積，與代謝症候群的引發相關。本研究採用自行合成的 100 nm 聚對苯二甲酸乙二酯（polyethylene terephthalate, PET）及商業 250 nm 聚乳酸（poly lactic acid, PLA）兩種與塑膠食品接觸材料相關的材質，來探討不同奈米塑膠種類對脂肪細胞的影響。首先對於奈米塑膠的粒徑、型態、界達電位、親脂性、染料釋出性進行微粒物化特性的分析，其次使用已分化為脂肪細胞的 3T3-L1 細胞，觀察細胞攝取微粒的速率、攝取量及攝取機制。最後探討奈米塑膠是否能夠影響脂肪細胞油滴的生成及發炎因子的釋放。實驗結果顯示 PET 塑膠微粒可透過網格蛋白調節的胞吞作用和巨胞飲作用進入溶?體中，24 小時暴露後平均每個細胞攝入12014 ± 2356 顆 PET。當塑膠微粒暴露於最高劑量（5×109 #/cm2）的 PET 時，細胞內的三酸甘油酯含量下降，然而暴露於劑量 1×107 #/cm2的 PET 時，荷爾蒙敏感型脂肪?（p-HSL/HSL）的蛋白表現比例下降。此外，雖然 PLA 塑膠微粒對於脂質的積累、脂解蛋白的調控皆無顯著影響，但暴露濃度 1×109 #/cm2 的PLA 時，脂肪合成相關蛋白硬脂醯輔? A 去飽和? （SCD-1）表現量會上升。總而言之，在本研究使用的劑量下雖然沒有觀察到奈米塑膠對脂肪細胞造成任何細胞毒性或發炎反應，但是對於脂質的代謝可造成一定的干擾。
Recently, micro/nanoplastics have been found in the natural environment, marine organisms, and condiments (sugar, salt, honey), and even plastic food contact materials such as tea bags or milk bottles can release a large amount of invisible plastic particles when they contact with hot water. Human beings are inevitably exposed to plastic particles through ingestion or inhalation, and therefore, the issue of its impact on human health has attracted attention. However, more research has been conducted on microplastics, while there is a lack of research on the biological effects of nanoplastics. Limited evidence showed that nanoplastics might accumulate in fat tissue and affected lipid metabolism. Therefore, nanoplastics may act as an environmental factor to promote the formation and accumulation of fat, potentially causing metabolic syndrome. In this study, two types of plastic food contact material related nanoplastics, self-synthesized 100 nm polyethylene terephthalate (PET) and commercial 250 nm poly lactic acid (PLA), were used to investigate the effects of different types of nanoplastics on adipocytes. The size, morphology, zeta potential, lipophilicity and dye leakage of the nanoplastics were measured, and then the uptake quantification/pathways and localization of nanoplastics were studied in differentiated 3T3-L1 adipocytes. Finally, lipid accumulation, lipogenesis/lipolysis pathways and cytokines release were studied. Results showed that PET nanoplastics was taken up by cells through clathrin-dependent endocytosis and micropinocytosis with an average uptake of 12014 ± 2356 particles per cell after 24 h. At the highest dose (5×109 #/cm2), PET treatment decreased triglycerides content. However, at a dose of 1×107 #/cm2, expression of lipolysis-related protein phosphate hormone sensitive lipase/hormone sensitive lipase (p-HSL/HSL) decreased. Although PLA nanoplastics had no significant effect on either lipid accumulation or lipolysis in this study, the protein expression of lipogenesis related stearoyl-CoA desaturase (SCD-1) increased at a dose of 1×109 #/cm2. In conclusion, although there’s no cytotoxicity or inflammation caused by nanoplastics to adipocytes, they still caused certain disruption in lipid metabolism. |
