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Assessing the toxicity of 17α-ethinylestradiol in rainbow trout using a four-day transcriptomics benchmark dose (BMD) embryo assay

ABSTRACT: Assessing the toxicity of 17α-ethinylestradiol in rainbow trout using a four-day transcriptomics benchmark dose (BMD) embryo assay

PROVIDER: PRJNA720912 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14197332_1.fastq.gz	Fastqsanger.gz
	SRR14197332_2.fastq.gz	Fastqsanger.gz
	SRR14197333_1.fastq.gz	Fastqsanger.gz
	SRR14197333_2.fastq.gz	Fastqsanger.gz
	SRR14197334_1.fastq.gz	Fastqsanger.gz

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Assessing the toxicity of 17α-ethinylestradiol in rainbow trout using a four-day transcriptomics benchmark dose (BMD) embryo assay

Project description:There is an urgent demand for more efficient and ethical approaches in chemical risk assessment. Using 17α-ethinylestradiol (EE2) as a model compound, this study established a live-animal alternative embryo benchmark-dose (BMD) assay for rainbow trout (RBT; Oncorhynchus mykiss) to derive transcriptomic points-of-departure (tPODs). Embryos were exposed to graded concentrations of EE2 (0, 1.13, 1.57, 6.22, 16.3, 55.1, and 169 ng/L) from hatch to 4 and up to 60 days post-hatch (dph) to assess molecular and apical responses, respectively. Whole proteome analyses of alevins did not show clear estrogenic effects, while transcriptomics revealed responses that were in agreement with apical effects including excessive accumulation of intravascular and hepatic proteinaceous fluid and significant increases in mortality at 55.1 and 169 ng/L EE2 at later time points. Transcriptomic BMD analysis estimated the median of the 20th lowest geneBMD to be 0.18 ng/L; the most sensitive tPOD. Other estimates (0.78, 3.64, and 1.63 ng/L for the tenth percentile geneBMD, first peak geneBMD distribution, and median geneBMD of the most sensitive overrepresented pathway, respectively) were within the same order of magnitude as empirically derived apical P ODs for EE2 in the literature. This 4-day alternative RBT embryonic assay was effective in deriving protective tPODs for EE2.

2021-08-17 | GSE171788 | GEO

Transcriptomic points-of-departure (tPOD) derived from a 4-day rainbow trout embryo toxicity test were protective of apical effects for 17α-ethinylestradiol

Project description:There is an urgent demand for more efficient and ethical approaches in chemical risk assessment. Using 17α-ethinylestradiol (EE2) as a model compound, this study established a live-animal alternative embryo benchmark-dose (BMD) assay for rainbow trout (RBT; Oncorhynchus mykiss) to derive transcriptomic points-of-departure (tPODs). Embryos were exposed to graded concentrations of EE2 (0, 1.13, 1.57, 6.22, 16.3, 55.1, and 169 ng/L) from hatch to 4 and up to 60 days post-hatch (dph) to assess molecular and apical responses, respectively. Whole proteome analyses of alevins did not show clear estrogenic effects, while transcriptomics revealed responses that were in agreement with apical effects including excessive accumulation of intravascular and hepatic proteinaceous fluid and significant increases in mortality at 55.1 and 169 ng/L EE2 at later time points. Transcriptomic BMD analysis estimated the median of the 20th lowest geneBMD to be 0.18 ng/L; the most sensitive tPOD. Other estimates (0.78, 3.64, and 1.63 ng/L for the tenth percentile geneBMD, first peak geneBMD distribution, and median geneBMD of the most sensitive overrepresented pathway, respectively) were within the same order of magnitude as empirically derived apical PODs for EE2 in the literature. This 4-day alternative RBT embryonic assay was effective in deriving protective tPODs for EE2.

2021-08-17 | PXD025251 | Pride

RNA-seq of the zebrafish (danio rerio) brain after developmental exposure to 17α-ethinylestradiol

Project description:RNA-seq of the zebrafish (danio rerio) brain after developmental exposure to 17α-ethinylestradiol

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Gene expression signatures for 17α-ethinylestradiol and ZM 189,154, singly and combined, in fathead minnow testis

Project description:Aquatic organisms are continuously exposed to complex mixtures of chemicals, many of which can interfere with their endocrine system, resulting in impaired reproduction, development or survival, among others. In order to analyze the effects and mechanisms of action of estrogen/anti-estrogen mixtures, we exposed male fathead minnows (Pimephales promelas) for 48 hours via the water to 2, 5, 10, and 50 ng 17α- ethinylestradiol (EE2)/L, 100 ng ZM 189,154/L (a potent antiestrogen known to block activity of all estrogen receptors) or mixtures of 5 or 50 ng EE2/L with 100 ng ZM 189,154/L. We analyzed gene expression changes in the gonad, as well as hormone and vitellogenin plasma levels. Steroidogenesis was down-regulated by EE2 as reflected by the reduced plasma levels of testosterone in the exposed fish and down-regulation of genes in the steroidogenic pathway. Microarray analysis of testis of fathead minnows treated with 5 ng EE2/L or with the mixture of 5 ng EE2/L and 100 ng ZM 189,154/L indicated that some of the genes whose expression was changed by EE2 were blocked by ZM 189,154, while others were either not blocked or enhanced by the mixture, generating two distinct expression patterns. Gene ontology and pathway analysis programs were used to determine categories of genes for each expression pattern. Our results suggest that response to estrogens occurs via multiple mechanisms, including canonical binding to soluble estrogen receptors, membrane estrogen receptors, and other mechanisms that are not blocked by pure antiestrogens.

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Development of a comprehensive toxicity pathway model for 17α-ethinylestradiol in early life stage fathead minnows (Pimephales promelas)

2021-04-09 | PXD021155 | Pride

Development of a comprehensive toxicity pathway model for 17α-ethinylestradiol (EE2) in early life stage fathead minnows (Pimephales promelas)

Project description:Development of a comprehensive toxicity pathway model for 17α-ethinylestradiol (EE2) in early life stage fathead minnows (Pimephales promelas)

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LC-MSMS of postmenopausal with low BMD

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