Developmental toxicity of hydroxylated chrysene metabolites in zebrafish embryos
| Autor: | Graciel Diamante, Norma Menjivar-Cervantes, David C. Volz, Daniel Schlenk, Afonso Celso Dias Bainy, Gabrielle do Amaral e Silva Müller, Elvis Genbo Xu |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Chrysene medicine.medical_specialty Embryo Nonmammalian medicine.drug_class Health Toxicology and Mutagenesis Organogenesis Developmental toxicity Estrogen receptor 010501 environmental sciences Aquatic Science 01 natural sciences Chrysenes 03 medical and health sciences chemistry.chemical_compound Internal medicine medicine Animals Zebrafish 0105 earth and related environmental sciences biology Dose-Response Relationship Drug Gene Expression Regulation Developmental Heart biology.organism_classification 030104 developmental biology Endocrinology Petroleum chemistry Estrogen Environmental chemistry Toxicity Signal transduction GPER Water Pollutants Chemical |
| Zdroj: | Aquatic toxicology (Amsterdam, Netherlands). 189 |
| ISSN: | 1879-1514 |
| Popis: | One of the primary sources of polycyclic aromatic hydrocarbons (PAHs) in marine environments is oil. Photochemical oxidation and microbial transformation of PAH-containing oils can result in the formation of oxygenated products. Among the PAHs in crude oil, chrysene is one of the most persistent within the water column and may be transformed to 2- and 6-hydroxychrysene (OHCHR). Both of these compounds have been shown to activate (2-OHCHR) and antagonize (6-OHCHR) the estrogen receptor (ER). Previous studies in our lab have shown that estrogen can significantly alter zebrafish development. However, little is known about the developmental toxicity of hydroxylated PAHs. Zebrafish embryos were exposed to 0.5-10μM of 2- or 6-OHCHR from 2h post-fertilization (hpf) until 76hpf. A significant decrease in survival was observed following exposure to 6-OHCHR - but not 2-OHCHR. Both OHCHRs significantly increased the percentage of overall deformities after treatment. In addition to cardiac malformations, ocular and circulatory defects were also observed in embryos exposed to both compounds, while 2-OHCHR generally resulted in a higher prevalence of effect. Moreover, treatment with 2-OHCHR resulted in a significant decrease in hemoglobin levels. ER nor G-Protein coupled estrogen receptor (GPER) antagonists and agonists did not rescue the observed defects. We also analyzed the expression of cardiac-, eye- and circulation-related genes previously shown to be affected by oil. Rhodopsin mRNA expresssion was significantly decreased by both compounds equally. However, exposure to 2-OHCHR significantly increased the expression of the hematopoietic regulator, runx1 (runt related transcription factor 1). These results indicate the toxicity of oxygenated photoproducts of PAHs and suggest that other targets and signaling pathways may contribute to developmental toxicity of weathered oil. Our findings also demonstrate the regio-selective toxicity of hydroxy-PAHs in the effects on eye and circulatory development and raise the need to identify mechanisms and ecological risks of oxy-PAHs to fish populations. |
| Databáze: | OpenAIRE |
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