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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 姜至剛 | zh_TW |
| dc.contributor.advisor | Chih-Kang Chiang | en |
| dc.contributor.author | 張永 | zh_TW |
| dc.contributor.author | Yung Chang | en |
| dc.date.accessioned | 2025-09-09T16:09:12Z | - |
| dc.date.available | 2025-09-10 | - |
| dc.date.copyright | 2025-09-09 | - |
| dc.date.issued | 2025 | - |
| dc.date.submitted | 2025-07-02 | - |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/99360 | - |
| dc.description.abstract | 鉈（Thallium, Tl）廣泛應用於半導體、成像系統、光纖玻璃與高溫超導材料等領域，近年來於全球多處地表水中被檢測，濃度最高可達1520 μg/L。鉈在水體中以穩定的一價形式（Tl⁺）存在，並展現超過10,000的生物濃縮係數。魚類與蔬菜中均可檢測出高濃度鉈殘留，顯示其於食物鏈中高度累積。作為食物鏈頂層的消費者，人類面臨鉈暴露的高度風險。即使在低劑量下，鉈亦與早產與發育異常相關，對兒童及孕婦等脆弱族群尤具威脅。儘管鉈的毒理機制尚未完全釐清，已有研究顯示其可誘發內質網壓力（ER stress），上調未摺疊蛋白反應（UPR）相關標誌如ATF6、IRE1，並促進XBP1剪接進入細胞核，導致細胞毒性。鑒於適應性UPR可能參與調節鉈所致毒性，本研究以斑馬魚為水生脊椎動物模式，探討鉈對胚胎發育之毒性機轉，以及選擇性XBP1活化劑IXA4之保護潛力，並與化學伴護劑TUDCA進行比較。
本研究建立鉈（Tl）誘導之斑馬魚毒性模型，結果顯示，隨鉈濃度上升，仔魚於120 hpf時的死亡率顯著增加，孵化率則明顯下降。形態學分析指出，在100–400 μg/L下魚鰾面積明顯縮小，且於200–400 μg/L濃度間觀察到心包腫脹與腹部異常，導致整體形態評分隨濃度提升而下降。qPCR分析顯示，鉈暴露顯著上調UPR標誌基因表現，反映出明確的內質網壓力反應。進一步以20 μM IXA4或TUDCA處理後，斑馬魚胚胎於6–144 hpf 期間之死亡率與對照組無顯著差異，顯示兩者本身無發育毒性。但在鉈處理下，單獨鉈暴露組的120 hpf存活率僅為53%，聯合IXA4或TUDCA處理則可顯著提升至79%與73%，並有效改善孵化率。組織學分析進一步發現，鉈會導致心包腫脹與腦部發育異常，而IXA4可顯著改善心臟與神經組織結構，展現器官層級的保護作用。轉錄體與生物資訊分析顯示，鉈暴露顯著抑制多條與心臟與神經發育相關之基因表現路徑，IXA4可部分恢復其轉錄活性，並上調DNA修復路徑，特別是核苷酸切除修復（NER）相關基因，其變化亦經qPCR驗證支持。 本研究顯示，選擇性sXBP1活化劑IXA4可透過促進DNA修復機制、調控心臟與神經發育相關基因表現，以及降低內質網壓力，顯著緩解鉈所誘導之發育毒性與器官損傷，為揭示鉈毒性機轉與未來治療策略的發展提供關鍵見解。 | zh_TW |
| dc.description.abstract | Thallium (Tl) is widely used in semiconductors, imaging systems, fiber optic glass, and high-temperature superconducting materials. In recent years, it has been detected in surface water across many regions of the world, with concentrations reaching up to 1520 μg/L. In aquatic environments, thallium exists in a stable monovalent form (Tl⁺) and exhibits a bioconcentration factor exceeding 10,000. High levels of thallium residues have been detected in both fish and vegetables, indicating its high accumulation within the food chain. As apex consumers, humans face a high risk of thallium exposure. Even at low doses, thallium has been associated with preterm birth and developmental abnormalities, posing a particular threat to vulnerable populations such as children and pregnant women. Although the toxicological mechanisms of thallium are not yet fully understood, studies have shown that it can induce endoplasmic reticulum (ER) stress, upregulate unfolded protein response (UPR) markers such as ATF6 and IRE1, and promote XBP1 splicing and nuclear translocation, leading to cytotoxicity. Given that adaptive UPR may be involved in regulating thallium-induced toxicity, this study used zebrafish as an aquatic vertebrate model to investigate the developmental toxicity mechanisms of thallium and the protective potential of the selective XBP1 activator IXA4, in comparison with the chemical chaperone TUDCA.
In this study, a zebrafish toxicity model induced by thallium (Tl) was established. Results showed that with increasing thallium concentration, the mortality rate of larvae at 120 hpf significantly increased, while the hatching rate markedly decreased. Morphological analysis revealed that at concentrations of 100–400 μg/L, the swim bladder area was significantly reduced, and pericardial edema and abdominal abnormalities were observed at 200–400 μg/L, resulting in a concentration-dependent decline in overall morphological scores. qPCR analysis showed that thallium exposure significantly upregulated UPR marker gene expression, indicating a clear ER stress response. Further treatment with 20 μM IXA4 or TUDCA during the 6–144 hpf period showed no significant differences in mortality compared to the control group, indicating no developmental toxicity from either compound alone. However, under thallium exposure, the 120 hpf survival rate in the thallium-only group was only 53%, while co-treatment with IXA4 or TUDCA significantly increased survival to 79% and 73%, respectively, and effectively improved the hatching rate. Histological analysis further revealed that thallium caused pericardial edema and abnormal brain development, while IXA4 significantly improved the structure of cardiac and neural tissues, demonstrating organ-level protective effects. Transcriptomic and bioinformatic analyses showed that thallium exposure significantly suppressed multiple gene expression pathways related to cardiac and neural development. IXA4 partially restored transcriptional activity and upregulated DNA repair pathways, particularly nucleotide excision repair (NER)-related genes, which was also supported by qPCR validation. This study demonstrates that the selective sXBP1 activator IXA4 can significantly alleviate thallium-induced developmental toxicity and organ damage by enhancing DNA repair mechanisms, regulating gene expression related to cardiac and neural development, and reducing ER stress. These findings provide critical insights into the mechanisms of thallium toxicity and the development of future therapeutic strategies. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2025-09-09T16:09:12Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2025-09-09T16:09:12Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | 口試委員審定書 I
謝辭 II 摘要 IV Abstract V Contents VII List of Figures XI List of Tables XIII Chapter 1 Introduction 1 1.1 Basic Properties and Minerals of Thallium 1 1.1.1 Thallium Deposits 2 1.1.2 Thallium Minerals and Their Geochemical Occurrence 5 1.2 Applications of Thallium 6 1.3 Thallium in the Environment 7 1.3.1 Thallium Contamination in Aquatic Environments 7 1.4 Thallium Exposure in Daily Life 9 1.4.1 Thallium in Beverages 9 1.4.2 Thallium in Tobacco 10 1.4.3 Thallium in Vegetables 11 1.5 Epidemiological Investigations of Thallium Exposure 14 1.5.1 Impact of Thallium on Human Renal Health 14 1.5.2 Effects of Thallium on the Health of Children and Pregnant Women 17 1.5.3 Effects of Thallium on the Health of Smokers 21 1.5.4 Thallium-Related Neuropsychological, Metabolic, and Other Health Effects 24 1.6 Molecular Toxicity and Adverse Effects of Thallium 27 1.6.1 Mitochondria-Mediated Oxidative Stress Induced by Thallium 27 1.6.2 Thallium-Induced Cytotoxicity via Endoplasmic Reticulum Stress 34 1.6.3 Genotoxicity and Other Adverse Effects of Thallium 36 1.7 Thallium Studies in Animal Models 40 1.7.1 Toxicity and Adverse Effects of Thallium in Mammalian Models 40 1.7.2 Thallium Toxicity and Adverse Effects in the Zebrafish Model 44 1.8 Unfolded Protein Response (UPR) in the Endoplasmic Reticulum 49 1.8.1 IRE1-XBP1 Pathway 51 1.8.2 ATF6 Pathway 51 1.8.3 PERK Pathway 52 1.9 IXA4-IRE1/XBP1s Activator 53 Chapter 2 Aim 55 2.1 Rationale 55 2.2 Hypothesis 55 2.3 Specific Aims 56 Chapter 3 Materials and Methods 57 3.1 Zebrafish Husbandry and Maintenance 57 3.2 Preparation of Chemical Solutions 57 3.3 Thallium (Tl) and Chemicals Exposure to Zebrafish 57 3.4 Survival and Hatching Rates 58 3.5 Blood Flow Measurement 58 3.6 Locomotor Activity Analysis 59 3.7 Analysis of Cardiac Morphology and Sinus Venosus–Bulbus Arteriosus Distance 59 3.8 Morphological Assessment 60 3.9 Histological Analysis 60 3.10 RNA Sequencing (RNA-seq) and Bioinformatic Analysis 60 3.11 Quantitative RT-PCR (qPCR) 61 3.12 Statistical Analysis 62 Chapter 4 Result and Discussion 63 4.1 Result 63 4.1.1 Experimental Design Overview 63 4.1.2 Early Developmental Toxicity of Tl Exposure 63 4.1.3 Morphological Defects and Abdominal Enlargement Following Tl Exposure 64 4.1.4 Thallium Exposure Impairs Blood Flow Activity and Locomotor Behavior 65 4.1.5 Thallium Exposure Disrupts Cardiac Morphology and Chamber Patterning 65 4.1.6 Thallium Exposure Activates Unfolded Protein Response (UPR)–Related Gene Expression 66 4.1.7 IXA4 and TUDCA Attenuate Tl-Induced Developmental Toxicity in Zebrafish 66 4.1.8 TUDCA and IXA4 alleviate thallium-induced morphological abnormalities in zebrafish embryos 67 4.1.9 IXA4 and TUDCA Protect Against Tl-Induced Structural Defects in the Brain and Heart 68 4.1.10 Transcriptomic Analysis Reveals that IXA4 and TUDCA Mitigate Tl-Induced Gene Expression Dysregulation 68 4.1.11 Gene Set Enrichment Reveals Tl Disrupts Mitochondrial and Developmental Pathways 69 4.1.12 Transcriptomic Enrichment Analysis Reveals Tl-induced Suppression of Neural and Cardiovascular Development 70 4.1.13 Co-Treatment with IXA4 and TUDCA Partially Rescues Tl-Induced Gene Expression Changes in Neural and Cardiac Markers 70 4.1.14 IXA4 Modulates NER- and Neurodevelopment-Related Gene Sets Suppressed by Tl Exposure 71 4.1.15 IXA4 Restores DNA Repair Gene Expression Suppressed by Tl Exposure 71 4.2 Discussion 72 Chapter 5 Conclusion and Future Perspective 78 Figures 80 Tables 96 References 98 Appendix: Publications During Doctoral Study 119 | - |
| dc.language.iso | en | - |
| dc.subject | 鉈 | zh_TW |
| dc.subject | 斑馬魚胚胎模型 | zh_TW |
| dc.subject | 適應性未摺疊蛋白反應 | zh_TW |
| dc.subject | IXA4 | zh_TW |
| dc.subject | 轉錄體分析 | zh_TW |
| dc.subject | DNA修復 | zh_TW |
| dc.subject | embryonic zebrafish model | en |
| dc.subject | Thallium | en |
| dc.subject | transcriptomic profiling | en |
| dc.subject | DNA repair | en |
| dc.subject | adaptive unfolded protein response (UPR) | en |
| dc.subject | IXA4 | en |
| dc.title | 鉈誘發斑馬魚神經與心臟毒性：適應性未摺疊蛋白反應與DNA修復機制的保護作用 | zh_TW |
| dc.title | Thallium-Induced Neurocardiotoxicity in Zebrafish: Protective Role of Adaptive UPR and DNA Repair | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 113-2 | - |
| dc.description.degree | 博士 | - |
| dc.contributor.oralexamcommittee | 劉興華;趙家德;王一中;孫樵隱 | zh_TW |
| dc.contributor.oralexamcommittee | SHING-HWA LIU;Chia-Ter Chao;I-JONG WANG;Chiao-Yin Sun | en |
| dc.subject.keyword | 鉈,斑馬魚胚胎模型,適應性未摺疊蛋白反應,IXA4,轉錄體分析,DNA修復, | zh_TW |
| dc.subject.keyword | Thallium,embryonic zebrafish model,adaptive unfolded protein response (UPR),IXA4,transcriptomic profiling,DNA repair, | en |
| dc.relation.page | 119 | - |
| dc.identifier.doi | 10.6342/NTU202501211 | - |
| dc.rights.note | 同意授權(限校園內公開) | - |
| dc.date.accepted | 2025-07-03 | - |
| dc.contributor.author-college | 醫學院 | - |
| dc.contributor.author-dept | 毒理學研究所 | - |
| dc.date.embargo-lift | 2030-06-18 | - |
| 顯示於系所單位： | 毒理學研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-113-2.pdf 未授權公開取用 | 3.95 MB | Adobe PDF | 檢視/開啟 |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。