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Embryo/ larval toxicity and key gene expression signatures of maternally transferred hexabromocyclododecane (HBCD) in Pimephales promelas

ABSTRACT: Embryo/ larval toxicity and key gene expression signatures of maternally transferred hexabromocyclododecane (HBCD) in Pimephales promelas

PROVIDER: PRJNA874903 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21314752_1.fastq.gz	Fastqsanger.gz
	SRR21314752_2.fastq.gz	Fastqsanger.gz
	SRR21314753_1.fastq.gz	Fastqsanger.gz
	SRR21314753_2.fastq.gz	Fastqsanger.gz
	SRR21314754_1.fastq.gz	Fastqsanger.gz

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Embryo/ larval toxicity and key gene expression signatures of maternally transferred hexabromocyclododecane (HBCD) in Pimephales promelas

Project description:Hexabromocyclododecane (HBCD) is a brominated flame retardant that presents a threat to aquatic organisms as it can be maternally transferred and has been reported to hinder development and survival in early-life stage (ELS) fish. However, little is known to date regarding the molecular mechanisms that drive the toxicity of HBCD. This study examined the apical and molecular response patterns of maternally transferred HBCD in fathead minnow (Pimephales promelas) larvae at seven (whole transcriptome) and 14 (apical and physiological) days post-fertilization. The larvae sampled at 7dpf for whole transcriptomics analysis revealed dysregulation of pathways involved in membrane integrity (inhibition of calcium channel) and metabolic processes (downregulation of amino acid, glucose, and lipid biosynthesis), while the larvae reared for 14 days exhibited a significant decrease in survival at the highest treatment condition. These results indicate that maternal transfer of HBCD is of concern in fish, which may act through indirect mechanisms involving the inhibition of membrane transport leading to disruption in metabolic processes, collectively resulting in energy depletion and subsequently mortality.

2022-09-02 | GSE212295 | GEO

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