The toxicity of guaiacol on craniofacial cartilage development through ROS-induced oxidative stress in zebrafish embryos
The combustion of biomass (e.g., wood, agricultural residues) and coal releases significant amounts of guaiacol (GUA) and its derivatives, major constituents of PM2.5 that threaten human health and ecosystems. GUA can rapidly enter the Earth's water circulation system through atmospheric deposi...
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| Format: | Article |
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Elsevier
2025-09-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651325010899 |
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| author | Xianhua Zhang Runfa Wu Fasheng Liu Min Huang Xiaoyan Huang Nannan Wang Qianqian Huang Minhong Zhang Xinjun Liao Huiqiang Lu Lan Liao |
| author_facet | Xianhua Zhang Runfa Wu Fasheng Liu Min Huang Xiaoyan Huang Nannan Wang Qianqian Huang Minhong Zhang Xinjun Liao Huiqiang Lu Lan Liao |
| author_sort | Xianhua Zhang |
| collection | DOAJ |
| description | The combustion of biomass (e.g., wood, agricultural residues) and coal releases significant amounts of guaiacol (GUA) and its derivatives, major constituents of PM2.5 that threaten human health and ecosystems. GUA can rapidly enter the Earth's water circulation system through atmospheric deposition. However, its potential threat to aquatic organism and humans remains poorly understood. Using zebrafish—a model organism with high genetic homology to humans, transparent embryos, and rapid development—we investigated GUA’s ecological effects. Zebrafish embryos were exposed to 0.08–0.24 mM GUA from 12 to 120 h post-fertilization (hpf). GUA induced craniofacial malformations, behavioral abnormalities (reduced locomotion, impaired stimuli response), and oxidative stress via reactive oxygen species (ROS) accumulation. Disrupted migration, proliferation, and differentiation of cranial neural crest cells (NCCs) were observed, alongside altered Wnt signaling pathway gene expression. Both astaxanthin (AST, an ROS scavenger) and C59 (a Wnt inhibitor) could mitigate craniofacial defects. These findings demonstrate that GUA reduces antioxidant capacity, impairs NCCs function, and disrupts Wnt signaling, leading to craniofacial deformities. This study highlights GUA’s ecological and health risks, providing insights into its toxic mechanisms. |
| format | Article |
| id | doaj-art-5773b5e7629c4e95b6260e8d92e90411 |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-5773b5e7629c4e95b6260e8d92e904112025-08-20T03:41:31ZengElsevierEcotoxicology and Environmental Safety0147-65132025-09-0130211874410.1016/j.ecoenv.2025.118744The toxicity of guaiacol on craniofacial cartilage development through ROS-induced oxidative stress in zebrafish embryosXianhua Zhang0Runfa Wu1Fasheng Liu2Min Huang3Xiaoyan Huang4Nannan Wang5Qianqian Huang6Minhong Zhang7Xinjun Liao8Huiqiang Lu9Lan Liao10The Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Provincial Clinical Research Center for Oral Diseases, Nanchang, Jiangxi 330006, ChinaThe Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Provincial Clinical Research Center for Oral Diseases, Nanchang, Jiangxi 330006, ChinaJiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Developmental Biology of Organs and Epigenetics, Clinical Research Center of Affiliated Hospital of Jinggangshan University, Affiliated Hospital of Jinggangshan University, Ji'an, Jiangxi 343009, ChinaThe Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Provincial Clinical Research Center for Oral Diseases, Nanchang, Jiangxi 330006, ChinaJiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Developmental Biology of Organs and Epigenetics, Clinical Research Center of Affiliated Hospital of Jinggangshan University, Affiliated Hospital of Jinggangshan University, Ji'an, Jiangxi 343009, ChinaJiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Developmental Biology of Organs and Epigenetics, Clinical Research Center of Affiliated Hospital of Jinggangshan University, Affiliated Hospital of Jinggangshan University, Ji'an, Jiangxi 343009, ChinaJiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Developmental Biology of Organs and Epigenetics, Clinical Research Center of Affiliated Hospital of Jinggangshan University, Affiliated Hospital of Jinggangshan University, Ji'an, Jiangxi 343009, ChinaClinical Medical Research Center, First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, ChinaJiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Developmental Biology of Organs and Epigenetics, Clinical Research Center of Affiliated Hospital of Jinggangshan University, Affiliated Hospital of Jinggangshan University, Ji'an, Jiangxi 343009, ChinaClinical Medical Research Center, First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China; Corresponding author.The Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Provincial Clinical Research Center for Oral Diseases, Nanchang, Jiangxi 330006, China; Jiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Developmental Biology of Organs and Epigenetics, Clinical Research Center of Affiliated Hospital of Jinggangshan University, Affiliated Hospital of Jinggangshan University, Ji'an, Jiangxi 343009, China; Corresponding author at: The Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Provincial Clinical Research Center for Oral Diseases, Nanchang, Jiangxi 330006, China.The combustion of biomass (e.g., wood, agricultural residues) and coal releases significant amounts of guaiacol (GUA) and its derivatives, major constituents of PM2.5 that threaten human health and ecosystems. GUA can rapidly enter the Earth's water circulation system through atmospheric deposition. However, its potential threat to aquatic organism and humans remains poorly understood. Using zebrafish—a model organism with high genetic homology to humans, transparent embryos, and rapid development—we investigated GUA’s ecological effects. Zebrafish embryos were exposed to 0.08–0.24 mM GUA from 12 to 120 h post-fertilization (hpf). GUA induced craniofacial malformations, behavioral abnormalities (reduced locomotion, impaired stimuli response), and oxidative stress via reactive oxygen species (ROS) accumulation. Disrupted migration, proliferation, and differentiation of cranial neural crest cells (NCCs) were observed, alongside altered Wnt signaling pathway gene expression. Both astaxanthin (AST, an ROS scavenger) and C59 (a Wnt inhibitor) could mitigate craniofacial defects. These findings demonstrate that GUA reduces antioxidant capacity, impairs NCCs function, and disrupts Wnt signaling, leading to craniofacial deformities. This study highlights GUA’s ecological and health risks, providing insights into its toxic mechanisms.http://www.sciencedirect.com/science/article/pii/S0147651325010899GuaiacolChondrogenesisPharyngeal archOxidative stressWnt signaling pathway |
| spellingShingle | Xianhua Zhang Runfa Wu Fasheng Liu Min Huang Xiaoyan Huang Nannan Wang Qianqian Huang Minhong Zhang Xinjun Liao Huiqiang Lu Lan Liao The toxicity of guaiacol on craniofacial cartilage development through ROS-induced oxidative stress in zebrafish embryos Ecotoxicology and Environmental Safety Guaiacol Chondrogenesis Pharyngeal arch Oxidative stress Wnt signaling pathway |
| title | The toxicity of guaiacol on craniofacial cartilage development through ROS-induced oxidative stress in zebrafish embryos |
| title_full | The toxicity of guaiacol on craniofacial cartilage development through ROS-induced oxidative stress in zebrafish embryos |
| title_fullStr | The toxicity of guaiacol on craniofacial cartilage development through ROS-induced oxidative stress in zebrafish embryos |
| title_full_unstemmed | The toxicity of guaiacol on craniofacial cartilage development through ROS-induced oxidative stress in zebrafish embryos |
| title_short | The toxicity of guaiacol on craniofacial cartilage development through ROS-induced oxidative stress in zebrafish embryos |
| title_sort | toxicity of guaiacol on craniofacial cartilage development through ros induced oxidative stress in zebrafish embryos |
| topic | Guaiacol Chondrogenesis Pharyngeal arch Oxidative stress Wnt signaling pathway |
| url | http://www.sciencedirect.com/science/article/pii/S0147651325010899 |
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