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Integrated multi-omics analysis reveals the underlying molecular mechanism for developmental neurotoxicity of perfluorooctanesulfonic acid in zebrafish

ABSTRACT: Integrated multi-omics analysis reveals the underlying molecular mechanism for developmental neurotoxicity of perfluorooctanesulfonic acid in zebrafish

PROVIDER: PRJNA950976 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24036820_1.fastq.gz	Fastqsanger.gz
	SRR24036820_2.fastq.gz	Fastqsanger.gz
	SRR24036821_1.fastq.gz	Fastqsanger.gz
	SRR24036821_2.fastq.gz	Fastqsanger.gz
	SRR24036822_1.fastq.gz	Fastqsanger.gz

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Integrated multi-omics analysis reveals the underlying molecular mechanism for developmental neurotoxicity of perfluorooctanesulfonic acid in zebrafish

Project description:Limited studies on multi-omics have been conducted to comprehensively investigate the molecular mechanism underlying the developmental neurotoxicity of perfluorooctanesulfonic acid (PFOS). In this study, the locomotor behavior of zebrafish larvae was assessed under the exposure to 0.1–20 μM PFOS based on its reported neurobehavioral effect. After the number of zebrafish larvae was optimized for proteomics and metabolomics studies, three kinds of omics (i.e., transcriptomics, proteomics, and metabolomics) were carried out with zebrafish larvae exposed to 0.1, 1, 5, and 10 μM PFOS. More importantly, a data-driven integration of multi-omics was performed to elucidate the toxicity mechanism involved in developmental neurotoxicity. In a concentration-dependent manner, exposure to PFOS provoked hyperactivity and hypoactivity under light and dark conditions, respectively. Individual omics revealed that PFOS exposure caused perturbations in the pathways of neurological function, oxidative stress, and energy metabolism. Integrated omics implied that there were decisive pathways for axonal deformation, neuroinflammatory stimulation, and dysregulation of calcium ion signaling, which are more clearly specified for neurotoxicity. Overall, our findings broaden the molecular understanding of the developmental neurotoxicity of PFOS, for which multi-omics and integrated omics analyses are efficient for discovering the significant molecular pathways related to developmental neurotoxicity in zebrafish.

2023-04-04 | GSE228664 | GEO

Integrative multi-omics reveals analogous developmental neurotoxicity mechanisms between perfluorobutanesulfonic acid and perfluorooctanesulfonic acid in zebrafish

Project description:The molecular mechanism of perfluorobutanesulfonic acid (PFBS), an alternative to legacy perfluorooctanesulfonic acid (PFOS), remains to be understood. Therefore, we conducted a developmental toxicity evaluation on zebrafish embryos exposed to PFBS and PFOS and assessed neurobehavioral changes at concentrations below each point of departure (POD) determined by embryonic mortality. Using transcriptomics, proteomics, and metabolomics, biomolecular perturbations in response to PFBS were profiled and then integrated for comparison with those for PFOS. Although PFBS (7525.47 M POD) was approximately 700 times less toxic than PFOS (11.42 M POD), similar alteration in behavioral assessment and neurochemical analysis was observed at the corresponding ratios of low and high concentrations. Multi-omics analysis revealed that the PFBS neurotoxicity mechanism was associated with oxidative stress, lipid metabolism, and glycolysis/glucogenesis. The commonalities in developmental neurotoxicity-related mechanisms between PFBS and PFOS interconnected by knowledge-based integration of multi-omics included the calcium signaling pathway, lipid homeostasis, and primary bile acid biosynthesis. Despite being less toxic than PFOS, PFBS exhibited similar dysregulated molecular mechanisms, suggesting that chain length differences do not affect the intrinsic toxicity mechanism. Overall, carefully managing potential toxicity of PFBS can secure its status as an alternative to PFOS.

2023-04-04 | GSE228670 | GEO

Integrative multi-omics reveals analogous developmental neurotoxicity mechanisms between perfluorobutanesulfonic acid and perfluorooctanesulfonic acid in zebrafish

Project description:Integrative multi-omics reveals analogous developmental neurotoxicity mechanisms between perfluorobutanesulfonic acid and perfluorooctanesulfonic acid in zebrafish

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Acrylamide acute neurotoxicity in adult zebrafish

Project description:Acute exposure to acrylamide (ACR), a type-2 alkene, may lead to a ataxia, skeletal muscles weakness and numbness of the extremities in exposed human and laboratory animals. Recently, a zebrafish model for ACR neurotoxicity mimicking most of the pathophysiological processes described in mammalian models, was generated in 8 days post-fertilization larvae. In order to better understand the predictive value of the zebrafish larvae model of acute ACR neurotoxicity, in the present manuscript the ACR acute neurotoxicity has been characterized in the brain of adult zebrafish, and the results compared with those obtained with the whole-larvae. Although qualitative and quantitative analysis of the data shows important differences in the ACR effects between the adult brain and the whole-larvae, the overall effects of ACR in adult zebrafish, including a significant decrease in locomotor activity, altered expression of transcriptional markers of proteins involved in synaptic vesicle cycle, presence of ACR-adducts on cysteine residues of some synaptic proteins, and changes in the profile of some neurotransmitter systems, are similar to those described in the larvae. Thus, these results support the suitability of the zebrafish ACR acute neurotoxicity recently developed in larvae for screening of molecules with therapeutic value to treat this toxic neuropathy.

2018-10-19 | PXD008993 | Pride

Mechanism of cytarabine-induced neurotoxicity

Project description:Mechanism of cytarabine-induced neurotoxicity

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Transcriptome analysis reveals differences in developmental neurotoxicity mechanism of methyl-, ethyl-, and propyl- parabens in zebrafish embryos

Project description:Limited studies on comparison of developmental (neuro)toxicity of parabens have been conducted and unharmonized concentrations between phenotypic observations and transcriptomic analysis hamper understanding of their differential molecular mechanism. Developmental toxicity testing was conducted with commonly used methyl- (MtP), ethyl- (EtP) and propyl-paraben (PrP) in zebrafish embryos. Based on benchmark dose 5% (BMD5), embryonic mortality based-point of departure (M-PoD) values of three parabens were determined and changes in locomotor behavior were evaluated at concentrations of 0, M-PoD/50, M-PoD/10, and M-PoD in which transcriptomic analysis was conducted to explore the underlying neurotoxicity mechanism. Higher long-chained parabens were more toxic than short-chained parabens, as determined by M-PoD values of 154.1, 72.6, and 24.2 µM for MtP, EtP, and PrP, respectively. While exposure to EtP resulted in hyperactivity, no behavior effect was observed by MtP and PrP. Transcriptomics analysis revealed that abnormal behaviors in EtP-exposed group are associated with the distinctly enriched pathways in signal, transport, calcium ion binding, and metal-binding. In contrast, exposure to MtP and PrP mainly disrupted the membrane and transmembrane, which are closely linked to abnormal embryonic development rather than neurobehavior changes. According to the changes in expression of signature mRNAs, tentative transcriptomic-based PoD (T-PoD) values for each paraben were determined as MtP (2.68 µM), EtP (3.85 µM), and PrP (1.4 µM).

2023-08-07 | GSE239773 | GEO

Mechanism of cytarabine-induced neurotoxicity [HTGTS]

Project description:Mechanism of cytarabine-induced neurotoxicity [HTGTS]

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Modeling acrylamide acute neurotoxicity in zebrafish larvae

Project description:Background: Acrylamide (ACR) is a broadly spread neurotoxic chemical of public health concern, as occupational or environmental exposure of humans to ACR may lead to a synaptopathy characterized by ataxia, skeletal muscles weakness and numbness of the extremities. Currently, only the mildly affected patients undergo complete recovery, and identification of new molecules with therapeutic bioactivity against ACR acute neurotoxicity is urgently needed. Objectives: We aimed to develop a zebrafish model for human ACR neurotoxicity. Methods: Adverse effects have been assessed at different levels, including analysis of the motor function (basal locomotor activity, visual motor response, kinematic of the touch-evoked escape response), histopathological evaluation (toluidine blue and whole-mount immunofluorescence), analysis of neural transcriptional markers (qPCR), proteomic analysis (μLC-MS-MS) and neurotransmitters profile (LC-MS/MS). Results: Our results show that zebrafish mimics most of the pathophysiological processes described in humans and mammalian models. Motor function was altered, including the response to sudden changes in light intensity. Specific effects were found on the presynaptic nerve terminals at the neuromuscular junction level, but not on the axonal tracts or myelin sheath integrity. Transcriptional markers of proteins involved in synaptic vesicle cycle were selectively altered, and the proteomic analysis showed that ACR-adducts were formed on cysteine residues of some synaptic proteins. Finally, analysis of neurotransmitters profile showed a significant effect found on cholinergic and dopaminergic systems. Conclusions: Thus, the zebrafish model for ACR acute neurotoxicity is suitable to be used larvae for in vivo high-throughput screening of small molecule libraries for identifying new drugs against this synaptopathy.

2018-10-24 | PXD007169 | Pride