ArticleToxicological sciences : an official journal of the Society of Toxicology2010
TCDD induced pericardial edema and relative COX-2 expression in medaka (Oryzias Latipes) embryos.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 49 citations in OpenAlex.
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- Fine particulate matter‑induced cardiac developmental toxicity (Review).Experimental and therapeutic medicine · 2025Review
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- A comparative study on targeted gene expression in zebrafish and its gill cell line exposed to chlorpyrifos.In vitro cellular & developmental biology. Animal · 2024Article
- From the Cover: Embryonic Exposure to TCDD Impacts Osteogenesis of the Axial Skeleton in Japanese medaka, Oryzias latipes.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- AHR-related activities in a creosote-adapted population of adult atlantic killifish, Fundulus heteroclitus, two decades post-EPA superfund status at the Atlantic Wood Site, Portsmouth, VA USA.Aquatic toxicology (Amsterdam, Netherlands) · 2016Article
- Article
- Effect-directed analysis of Elizabeth River porewater: developmental toxicity in zebrafish (Danio rerio).Environmental toxicology and chemistry · 2014Article
- Involvement of COX2-thromboxane pathway in TCDD-induced precardiac edema in developing zebrafish.Aquatic toxicology (Amsterdam, Netherlands) · 2014Article
- Ahr2-dependence of PCB126 effects on the swim bladder in relation to expression of CYP1 and cox-2 genes in developing zebrafish.Toxicology and applied pharmacology · 2012Article
- Reproductive and developmental toxicity of dioxin in fish.Molecular and cellular endocrinology · 2012Review
- TCDD disrupts hypural skeletogenesis during medaka embryonic development.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- Molecular targets that link dioxin exposure to toxicity phenotypes.The Journal of steroid biochemistry and molecular biology · 2011Review
- Embryonic exposure to low concentration of bisphenol A affects the development of Oryzias melastigma larvae.Environmental science and pollution research international · 2011Article
- Role of zebrafish cytochrome P450 CYP1C genes in the reduced mesencephalic vein blood flow caused by activation of AHR2.Toxicology and applied pharmacology · 2011Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Exposure to dioxin and other aryl hydrocarbon receptor (AhR) ligands results in multiple, specific developmental cardiovascular phenotypes including pericardial edema and circulatory failure in small aquarium fish models. Although phenotypes are well described, mechanistic underpinnings for such toxicities remain elusive. Here we suggest that AhR activation results in stimulation of inflammation and "eicosanoid" pathways, which contribute to the observed developmental, cardiovascular phenotypes. We demonstrate that medaka embryos exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0.05-1 ppb) during early development result in a dose-related increase in the prevalence of pericardial edema and that this phenotype correlates with an increase in cyclooxygenase-2 (COX-2) gene expression. Those individuals exhibiting the edema phenotype had significantly greater COX-2 mRNA than their nonedematous cohort. Selective pharmacological inhibition of COX-2, with NS-398, and genetic knock down of COX-2 with a translation initiation morpholino significantly attenuated prevalence and severity of edema phenotype. Subsequently, exposures of medaka embryos to arachidonic acid (AA) resulted in recapitulation of the pericardial edema phenotype and significantly increased COX-2 expression only in those individuals exhibiting the edema phenotype compared with their nonedematous cohort. AA exposure does not result in significant induction of cytochrome P450 1A expression, suggesting that pericardial edema can be induced independent of AhR/aryl hydrocarbon receptor nuclear translocator/dioxin response element interactions. Results from this study demonstrate that developmental exposure to TCDD results in an induction of inflammatory mediators including COX-2, which contribute to the onset, and progression of heart dysmorphogenesis in the medaka model.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.