| 摘要: | 奈米塑膠微粒 (Nanoplastics, NPs)會累積於食物及飲水中而被人體攝入，並經由血液傳送至各個器官。研究指出，NPs除了造成腸道系統的傷害，也可能成為一種新型態的心血管疾病風險因子，且心臟功能與粒線體息息相關，若NPs干擾粒線體功能，心臟功能也會降低。因此，本實驗目的在於利用細胞模式探討奈米塑膠微粒是否會被H9C2細胞吸收，於細胞內分佈與粒線體的定位關係，進而了解NPs是否干擾粒線體功能與品質。分別給予不同濃度之聚苯乙烯奈米塑膠微粒 (Polystyrene Nanoplastics, PSNPs) 培養 H9C2細胞 24小時，進行毒性分析、PSNPs在細胞與粒線體之定位分析、細胞內化分析，並檢測細胞粒線體功能、氧化壓力及粒線體品質管控之相關基因表現是否受到影響。結果顯示，細胞存活率無顯著的影響，100 nm PSNPs主要聚集於胞內體或溶?體，且不會進入粒線體。此外，PSNPs的劑量與細胞內化含量呈現劑量效應。而PSNPs在高劑量下會改變粒線體超微結構，使得褶皺消失不明顯，於檢測粒線體能量代謝功能，也可見負面影響之趨勢，粒線體膜電位亦可觀察到受PSNPs影響而降低。對粒線體的動態平衡、細胞凋亡相關之基因表現也有明顯提高之趨勢。因此，100 nm PSNPs在24小時的介入下雖未對H9C2細胞產生立即的毒性傷害，也未能直接性地進入粒線體內部而干擾蛋白的功能，但仍會改變粒線體結構、功能和品質，表示PSNPs對心臟的潛在威脅不容小覷。
Nanoplastics (NPs) accumulated in food and drinking water will be ingested by humans, and transported to various organs through the bloodstream. Studies indicate that besides causing damage to the intestinal system, NPs may also become a new type of cardiovascular disease risk factor. Heart function is closely related to mitochondria, and if NPs impair mitochondrial function, heart function will also decline. Thus, the purpose of this study is to use a cell model to explore whether NPs have direct contact with mitochondria and whether they disturb mitochondrial function and quality. Different concentrations of Polystyrene Nanoplastics (PSNPs) were administered to H9C2 cells for 24 hours. Toxicity analysis, PSNPs localization within cells and mitochondria, cellular internalization analysis, and assessments of mitochondrial function, oxidative stress, and related gene expression for mitochondrial quality control were conducted. Results showed that cell viability was not significantly affected. 100 nm PSNPs primarily accumulated in endosome or lysosome and did not enter the mitochondria. Additionally, there was a dose-effect relationship between the PSNPs dosage and their internalization level within cells. At high doses, PSNPs altered mitochondrial ultrastructure, making cristae less distinct, and negatively impacted mitochondrial energy metabolism functions, with a reduction in mitochondrial membrane potential. There were also noticeable increases in the expression of genes related to mitochondrial dynamics and apoptosis. Therefore, while 100 nm PSNPs did not cause immediate toxicity to H9C2 cells or directly interfere with mitochondrial within 24 hours, they did alter mitochondrial structure, function, and quality, indicating the potential threat of PSNPs to the heart should not be underestimated. |
