Hexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos
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| Název: | Hexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos |
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| Autoři: | Deng, J, Yu, L, Liu, C, Yu, K, Shi, X, Yeung, LWY, Lam, PKS, Wu, RSS, Zhou, B |
| Zdroj: | Aquatic Toxicology. 93:29-36 |
| Informace o vydavateli: | Elsevier BV, 2009. |
| Rok vydání: | 2009 |
| Témata: | Male, 0301 basic medicine, Embryo, Nonmammalian, Apoptosis, 01 natural sciences, Apoptosis Regulatory Proteins - Biosynthesis - Genetics, Random Allocation, 03 medical and health sciences, Messenger - Biosynthesis - Genetics, Animals, Hydrocarbons, Brominated - Toxicity, RNA, Messenger, Gene Expression Regulation, Developmental - Drug Effects, Flame Retardants - Toxicity, Zebrafish, Zebrafish - Embryology - Genetics, Flame Retardants, 0105 earth and related environmental sciences, Embryo, Nonmammalian - Drug Effects, Nonmammalian - Drug Effects, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Apoptosis - Drug Effects - Genetics, Abnormalities, Drug-Induced, Gene Expression Regulation, Developmental, Brominated - Toxicity, Rna, Messenger - Biosynthesis - Genetics, Abnormalities, Drug-Induced - Etiology, Drug-Induced - Etiology, Hydrocarbons, Hydrocarbons, Brominated, 3. Good health, Gene Expression Regulation, Embryo, Reactive Oxygen Species - Metabolism, Rna, Developmental - Drug Effects, Female, Abnormalities, Apoptosis Regulatory Proteins, Reactive Oxygen Species |
| Popis: | Hexabromocyclododecane (HBCD) is widely used as a brominated flame retardant, and has been detected in the aquatic environment, wild animals, and humans. However, details of the environmental health risk of HBCD are not well known. In this study, zebrafish embryos were used to assess the developmental toxicity of the chemical. Four-hour post-fertilization (hpf) zebrafish embryos were exposed to various concentrations of HBCD (0, 0.05, 0.1, 0.5, and 1.0 mg L(-1)) until 96 h. Exposure to 0.1, 0.5, and 1.0 mg L(-1) HBCD significantly increased the malformation rate and reduced survival in the 0.5 and 1.0 mg L(-1) HBCD exposure groups. Acridine orange (AO) staining showed that HBCD exposure resulted in cell apoptosis. Reactive oxygen species (ROS) was significantly induced at exposures of 0.1, 0.5, and 1.0 mg L(-1) HBCD. To test the apoptotic pathway, several genes related to cell apoptosis, such as p53, Puma, Apaf-1, caspase-9, and caspase-3, were examined using real-time PCR. The expression patterns of these genes were up-regulated to some extent. Two anti-apoptotic genes, Mdm2 (antagonist of p53) and Bcl-2 (inhibitor of Bax), were down-regulated, and the activity of capspase-9 and caspase-3 was significantly increased. The overall results demonstrate that waterborne HBCD is able to produce oxidative stress and induce apoptosis through the involvement of caspases in zebrafish embryos. The results also indicate that zebrafish embryos can serve as a reliable model for the developmental toxicity of HBCD. |
| Druh dokumentu: | Article |
| Jazyk: | English |
| ISSN: | 0166-445X |
| DOI: | 10.1016/j.aquatox.2009.03.001 |
| Přístupová URL adresa: | https://pubmed.ncbi.nlm.nih.gov/19356805 https://www.sciencedirect.com/science/article/pii/S0166445X09001003 http://www.diva-portal.org/smash/record.jsf?pid=diva2:950413 http://oru.diva-portal.org/smash/record.jsf?pid=diva2:950413 https://www.cabdirect.org/cabdirect/abstract/20093319504 http://www.sciencedirect.com/science/article/pii/S0166445X09001003 https://core.ac.uk/display/38013784 http://hdl.handle.net/10722/179136 |
| Rights: | Elsevier TDM |
| Přístupové číslo: | edsair.doi.dedup.....ad1f3d9dfa4102f929fc30a052d200dd |
| Databáze: | OpenAIRE |
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Nájsť tento článok vo Web of Science | Abstrakt: | Hexabromocyclododecane (HBCD) is widely used as a brominated flame retardant, and has been detected in the aquatic environment, wild animals, and humans. However, details of the environmental health risk of HBCD are not well known. In this study, zebrafish embryos were used to assess the developmental toxicity of the chemical. Four-hour post-fertilization (hpf) zebrafish embryos were exposed to various concentrations of HBCD (0, 0.05, 0.1, 0.5, and 1.0 mg L(-1)) until 96 h. Exposure to 0.1, 0.5, and 1.0 mg L(-1) HBCD significantly increased the malformation rate and reduced survival in the 0.5 and 1.0 mg L(-1) HBCD exposure groups. Acridine orange (AO) staining showed that HBCD exposure resulted in cell apoptosis. Reactive oxygen species (ROS) was significantly induced at exposures of 0.1, 0.5, and 1.0 mg L(-1) HBCD. To test the apoptotic pathway, several genes related to cell apoptosis, such as p53, Puma, Apaf-1, caspase-9, and caspase-3, were examined using real-time PCR. The expression patterns of these genes were up-regulated to some extent. Two anti-apoptotic genes, Mdm2 (antagonist of p53) and Bcl-2 (inhibitor of Bax), were down-regulated, and the activity of capspase-9 and caspase-3 was significantly increased. The overall results demonstrate that waterborne HBCD is able to produce oxidative stress and induce apoptosis through the involvement of caspases in zebrafish embryos. The results also indicate that zebrafish embryos can serve as a reliable model for the developmental toxicity of HBCD. |
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| ISSN: | 0166445X |
| DOI: | 10.1016/j.aquatox.2009.03.001 |