工程用奈米粒子如奈米二氧化鈦及奈米金已廣泛被運用在化妝品、塗料、太陽電池、生物感測器以及生物顯影等。因此，奈米粒子毒性評估日趨重要。
本研究我們利用模式生物秀麗隱桿線蟲來探討銳鈦礦及金紅石相二氧化鈦奈米粒子的毒性。實驗結果顯示秀麗隱桿線蟲可以攝入FITC修飾過的二氧化鈦奈米粒子，並藉由穿透式電子顯微鏡發現銳鈦礦及金紅石相二氧化鈦奈米粒子存在神經細胞體之細胞質中。
根據實驗數據指出，二氧化鈦奈米粒子會造成神經之軸突明顯變短，因此我們推測，二氧化鈦奈米粒子所造成之軸突變短進而造成蟲體運動行為的遲緩。此外，銳鈦礦相二氧化鈦奈米粒子並不會影響蟲體長度；然而實驗數據指出，蟲體的個體數在500 µg/ml濃度下的銳鈦礦相二氧化鈦奈米粒子反應72小時之後減少了50%。特別是金紅石相二氧化鈦奈米粒子對蟲體的長度跟個體數造成了負面的影響。由於蟲體無法進入L4階段導致蟲體數3天內降低為原來的一半。為了得到二氧化鈦奈米粒子中毒的細胞機制，我們使用DNA微陣列法來量測在二氧化鈦內米粒子暴露下基因表現量的改變。我們的數據顯示三個基因參與了金屬鍵結或金屬解毒(mtl-2, C45B2.2 及 nhr-247)，六個基因參與了繁殖力及生殖(mtl-2, F26F2.3, ZK970.7, clec-70, K08C9.7 及 C38C3.7)，四個基因參與了生長及形態發生(mtl-2, F26F2.3, C38C3.7及 nhr-247)，五個基因參與了神經的功能(C41G6.13, C45B2.2, srr-6, K08C9.7 及 C38C3.7)。
此外，我們利用尺寸可控制性的奈米金粒子來研究模式生物秀麗隱桿線蟲的基因毒理反應。我們證實了秀麗隱桿線蟲分別可以攝入有MUA修飾及沒有MUA修飾的奈米金粒子，而且可以由X光顯微技術偵測到蟲體腸道中含有這些金顆粒。在金粒子的暴露下秀麗隱桿線蟲的神經軸突變短了，這可能是導致蟲體運動行為遲緩的原因。此外，我們也測定出MUA對金粒子比例為0.5, 1 及 3的金粒子在72小時之後使蟲體數減少超過50%。再者，這些不同成分比例的金粒子也分別使體長、蠕動頻率以及後代數目降低。我們也利用了MTT法分析了暴露在金粒子下秀麗隱桿線蟲神經細胞的存活率。MUA對金粒子比例的增加降低了神經的存活率。為了進一步了解發育的變化以及基因表現量變化之間的關聯性，我們利用DNA微陣列法來量測基因表現量的變化(例如: clec-174參與了細胞的防護，cut-3 及 fil-1參與了形態發生，dpy-14表現在胚胎神經上，mtl-1參與了金屬解毒及體內平衡)。

Engineered nanoparticles such as TiO2 nanoparticles and gold nanoparticles are widely used in cosmetic, pigments, solar cells, biosensors, and bioimaging. Therefore, it is of critical importance to evaluate the toxicity of these nanoparticles.
In this study, we employed the model organism Caenorhabditis elegans to investigate the toxicology of anatase and rutile phase titanium dioxide (TiO2) nanoparticles (NPs). The results show that the nematode C. elegans can take up fluorescein isothiocyanate (FITC)-labeled TiO2 NPs and that both anatase and rutile TiO2 NPs can be detected in the cytoplasm of cultured primary C. elegans neurons by transmission electron microscopy (TEM). After TiO2 NPs exposure, these neurons grew significantly shorter axons, which may be related to the detected impeded worm locomotion behavior. Furthermore, anatase TiO2 NPs did not affect the worm’s body length; however, we determined that a concentration of 500 µg/ml anatase TiO2 NPs reduced a worm population by 50% within 72 hours. Notably, rutile TiO2 NPs negatively affect both body length and worm population. Our observations suggest that worms unable to enter L4 larval stages lead to a severe reduction in the worm population at TiO2 NPs of LC50/3d. In order to understand details of cellular mechanisms involved in TiO2 NPs intoxication, DNA microarray assays were employed to determine changes in gene expression in the presence or absence of TiO2 NPs exposure. Our data reveal TiO2 NPs exposure causes gene expression (RNA level) significant different from untreated worms displaying 3 metal binding/metal detoxification genes (mtl-2, C45B2.2 and nhr-247), 6 fertility/reproduction related genes (mtl-2, F26F2.3, ZK970.7, clec-70, K08C9.7 and C38C3.7), 4 worm growth/body morphogenesis associated genes (mtl-2, F26F2.3, C38C3.7 and nhr-247) and 5 genes with neuronal functions (C41G6.13, C45B2.2, srr-6, K08C9.7 and C38C3.7).
We also utilized size-tunable gold nanoparticles (Au NPs) to investigate the toxicogenomic responses of C. elegans. Here, we show that C. elegans can uptake Au NPs coated with or without 11-mercaptoundecanoic acid (MUA), and Au NPs are detectable in worm intestines using X-ray microscopy. After Au NP exposure, C. elegans neurons grew shorter axons, which may be related to the observed impeded worm locomotion. Furthermore, we determined that MUA to Au ratios of 0.5, 1 and 3 reduced the worm population by more than 50% within 72 hours. In addition, these MUA to Au ratios reduced the worm body size, thrashing frequencies (worm mobility) and brood size. MTT assays were then employed to analyze the viability of cultured C. elegans primary neurons exposed to MUA-Au NPs. Increasing the MUA to Au ratios increasingly reduced neuronal survival. To understand how developmental changes (after MUA-Au NP treatment) are related to changes in gene expression, we employed DNA microarray assays and identified changes in gene expression (e.g., clec-174, involved in cellular defense, cut-3 and fil-1, both involved in body morphogenesis, dpy-14, expressed in embryonic neurons, and mtl-1, functions in metal detoxification and homeostasis).

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