Effect of bisphenol A on craniofacial cartilage development in zebrafish (Danio rerio) embryos: A morphological study
Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal develo...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Huang, Wenlong [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021transfer abstract |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Erysipelas, the “Other” Cellulitis: A Practical Guide for Nurse Practitioners - Fetters, Lisa ELSEVIER, 2021, EES : official journal of the International Society of Ecotoxicology and Environmental safety, Amsterdam |
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| Übergeordnetes Werk: |
volume:212 ; year:2021 ; day:1 ; month:04 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.ecoenv.2021.111991 |
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| 245 | 1 | 0 | |a Effect of bisphenol A on craniofacial cartilage development in zebrafish (Danio rerio) embryos: A morphological study |
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| 520 | |a Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. | ||
| 520 | |a Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. | ||
| 650 | 7 | |a Bisphenol A |2 Elsevier | |
| 650 | 7 | |a Craniofacial cartilage development |2 Elsevier | |
| 650 | 7 | |a Endocrine-disrupting chemical |2 Elsevier | |
| 650 | 7 | |a Developmental toxicity |2 Elsevier | |
| 650 | 7 | |a Zebrafish |2 Elsevier | |
| 700 | 1 | |a Wang, Xin |4 oth | |
| 700 | 1 | |a Zheng, Shukai |4 oth | |
| 700 | 1 | |a Wu, Ruotong |4 oth | |
| 700 | 1 | |a Liu, Caixia |4 oth | |
| 700 | 1 | |a Wu, Kusheng |4 oth | |
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10.1016/j.ecoenv.2021.111991 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001353.pica (DE-627)ELV053103963 (ELSEVIER)S0147-6513(21)00102-0 DE-627 ger DE-627 rakwb eng 610 VZ 44.63 bkl Huang, Wenlong verfasserin aut Effect of bisphenol A on craniofacial cartilage development in zebrafish (Danio rerio) embryos: A morphological study 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A Elsevier Craniofacial cartilage development Elsevier Endocrine-disrupting chemical Elsevier Developmental toxicity Elsevier Zebrafish Elsevier Wang, Xin oth Zheng, Shukai oth Wu, Ruotong oth Liu, Caixia oth Wu, Kusheng oth Enthalten in Elsevier Fetters, Lisa ELSEVIER Erysipelas, the “Other” Cellulitis: A Practical Guide for Nurse Practitioners 2021 EES : official journal of the International Society of Ecotoxicology and Environmental safety Amsterdam (DE-627)ELV006765629 volume:212 year:2021 day:1 month:04 pages:0 https://doi.org/10.1016/j.ecoenv.2021.111991 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.63 Krankenpflege VZ AR 212 2021 1 0401 0 |
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10.1016/j.ecoenv.2021.111991 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001353.pica (DE-627)ELV053103963 (ELSEVIER)S0147-6513(21)00102-0 DE-627 ger DE-627 rakwb eng 610 VZ 44.63 bkl Huang, Wenlong verfasserin aut Effect of bisphenol A on craniofacial cartilage development in zebrafish (Danio rerio) embryos: A morphological study 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A Elsevier Craniofacial cartilage development Elsevier Endocrine-disrupting chemical Elsevier Developmental toxicity Elsevier Zebrafish Elsevier Wang, Xin oth Zheng, Shukai oth Wu, Ruotong oth Liu, Caixia oth Wu, Kusheng oth Enthalten in Elsevier Fetters, Lisa ELSEVIER Erysipelas, the “Other” Cellulitis: A Practical Guide for Nurse Practitioners 2021 EES : official journal of the International Society of Ecotoxicology and Environmental safety Amsterdam (DE-627)ELV006765629 volume:212 year:2021 day:1 month:04 pages:0 https://doi.org/10.1016/j.ecoenv.2021.111991 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.63 Krankenpflege VZ AR 212 2021 1 0401 0 |
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10.1016/j.ecoenv.2021.111991 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001353.pica (DE-627)ELV053103963 (ELSEVIER)S0147-6513(21)00102-0 DE-627 ger DE-627 rakwb eng 610 VZ 44.63 bkl Huang, Wenlong verfasserin aut Effect of bisphenol A on craniofacial cartilage development in zebrafish (Danio rerio) embryos: A morphological study 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A Elsevier Craniofacial cartilage development Elsevier Endocrine-disrupting chemical Elsevier Developmental toxicity Elsevier Zebrafish Elsevier Wang, Xin oth Zheng, Shukai oth Wu, Ruotong oth Liu, Caixia oth Wu, Kusheng oth Enthalten in Elsevier Fetters, Lisa ELSEVIER Erysipelas, the “Other” Cellulitis: A Practical Guide for Nurse Practitioners 2021 EES : official journal of the International Society of Ecotoxicology and Environmental safety Amsterdam (DE-627)ELV006765629 volume:212 year:2021 day:1 month:04 pages:0 https://doi.org/10.1016/j.ecoenv.2021.111991 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.63 Krankenpflege VZ AR 212 2021 1 0401 0 |
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10.1016/j.ecoenv.2021.111991 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001353.pica (DE-627)ELV053103963 (ELSEVIER)S0147-6513(21)00102-0 DE-627 ger DE-627 rakwb eng 610 VZ 44.63 bkl Huang, Wenlong verfasserin aut Effect of bisphenol A on craniofacial cartilage development in zebrafish (Danio rerio) embryos: A morphological study 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A Elsevier Craniofacial cartilage development Elsevier Endocrine-disrupting chemical Elsevier Developmental toxicity Elsevier Zebrafish Elsevier Wang, Xin oth Zheng, Shukai oth Wu, Ruotong oth Liu, Caixia oth Wu, Kusheng oth Enthalten in Elsevier Fetters, Lisa ELSEVIER Erysipelas, the “Other” Cellulitis: A Practical Guide for Nurse Practitioners 2021 EES : official journal of the International Society of Ecotoxicology and Environmental safety Amsterdam (DE-627)ELV006765629 volume:212 year:2021 day:1 month:04 pages:0 https://doi.org/10.1016/j.ecoenv.2021.111991 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.63 Krankenpflege VZ AR 212 2021 1 0401 0 |
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10.1016/j.ecoenv.2021.111991 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001353.pica (DE-627)ELV053103963 (ELSEVIER)S0147-6513(21)00102-0 DE-627 ger DE-627 rakwb eng 610 VZ 44.63 bkl Huang, Wenlong verfasserin aut Effect of bisphenol A on craniofacial cartilage development in zebrafish (Danio rerio) embryos: A morphological study 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. Bisphenol A Elsevier Craniofacial cartilage development Elsevier Endocrine-disrupting chemical Elsevier Developmental toxicity Elsevier Zebrafish Elsevier Wang, Xin oth Zheng, Shukai oth Wu, Ruotong oth Liu, Caixia oth Wu, Kusheng oth Enthalten in Elsevier Fetters, Lisa ELSEVIER Erysipelas, the “Other” Cellulitis: A Practical Guide for Nurse Practitioners 2021 EES : official journal of the International Society of Ecotoxicology and Environmental safety Amsterdam (DE-627)ELV006765629 volume:212 year:2021 day:1 month:04 pages:0 https://doi.org/10.1016/j.ecoenv.2021.111991 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.63 Krankenpflege VZ AR 212 2021 1 0401 0 |
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effect of bisphenol a on craniofacial cartilage development in zebrafish (danio rerio) embryos: a morphological study |
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Effect of bisphenol A on craniofacial cartilage development in zebrafish (Danio rerio) embryos: A morphological study |
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Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. |
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Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. |
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Bisphenol A (BPA), an endocrine-disrupting chemical, is present in everyday-used consumables and common household products. Although the side effects of BPA have been sufficiently explored, little is known the effects of environmentally relevant low levels of BPA on chondrogenesis in skeletal development. Here we used a morphological approach to investigate whether exposure to BPA (0, 0.0038, 0.05, 0.1, 1.0 μM) could affect craniofacial cartilage development of zebrafish embryo. Furthermore, we sought to determine receptor-mediated BPA induced chondrogenesis toxicity by co-exposing developing embryos to BPA and various inhibitors. Low-dose BPA affected heart rate and induced body and head elongation of larvae. Quantitative morphometric and histopathological analysis revealed that BPA exposure changed the angle and length of craniofacial cartilage elements and disrupted chondrocytes. BPA induced pharyngeal cartilage defects via multiple cellular pathways, including estrogen receptor, androgen receptor, and estrogen-related receptors. Our findings demonstrate that BPA alters the normal development of cartilage and craniofacial structures in zebrafish embryos. Furthermore, in this study we find multiple cellular pathways mediating the effects of BPA-induced craniofacial chondrogenesis toxicity. Further experiments will allow for establishing a connection between BPA and increased risk of congenital malformation of the facial cranium in BPA-exposed populations. |
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