J 2021

Disease network data for the pesticide fipronil in rat dopamine cells

SOUDERS, Christopher L.; Anna RUSHIN; Christina L. SANCHEZ; Darby TOTH; Ondřej ADAMOVSKÝ et al.

Basic information

Original name

Disease network data for the pesticide fipronil in rat dopamine cells

Authors

SOUDERS, Christopher L.; Anna RUSHIN; Christina L. SANCHEZ; Darby TOTH; Ondřej ADAMOVSKÝ and Christopher J. MARTYNIUK

Edition

Data in Brief, Amsterdam, Elsevier, 2021, 2352-3409

Other information

Language

English

Type of outcome

Article in a journal

Country of publisher

Netherlands

Confidentiality degree

is not subject to a state or trade secret

References:

Marked to be transferred to RIV

Yes

RIV identification code

RIV/00216224:14310/21:00122905

Organization

Přírodovědecká fakulta – Repository – Repository

EID Scopus

Keywords in English

Neurotoxicology; Pesticides; Alzheimer's disease; Gene expression; Interactome; Neurodegeneration

Links

EF17_043/0009632, research and development project. 857560, interní kód Repo. RECETOX RI, large research infrastructures.
Changed: 9/6/2025 00:50, RNDr. Daniel Jakubík

Abstract

In the original language

Transcriptome data were collected in rat dopamine cells exposed to fipronil for 24 h using microarray analysis. Fipronil is a phenylpyrazole pesticide that acts to inhibit gamma-aminobutyric acid (GABA), blocking inhibitory synaptic transmission in the central nervous system. Transcriptome data were subjected to pathway analysis and subnetwork enrichment analysis. We report that 25 mu M fipronil altered transcriptional networks in dopamine-synthesizing cells that are associated with Alzheimer's Disease, Huntington Disease, and Schizophrenia. Data analysis revealed that nerve fibre degeneration, nervous system malformations, neurofibrillary tangles, and neuroinflammation were all disease processes related to the transcriptome profile observed in the rat neuronal cells. Other disease networks altered by fipronil exposure at the transcript level were associated with the mitochondria, including mitochondrial DNA depletion syndrome and mitochondrial encephalomyopathies. These data, along with those presented in Souders et al. (2021), are significant because they increase understanding into the molecular mechanisms underlying human disease following exposures to neuroactive pesticides. These data can be reused to inform adverse outcome pathways for neurotoxic pesticides.

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