Přehled o publikaci
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
UT WoS
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.