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In vitro transcription studies used in a proof of concept whole transcriptome model predition study - HepaRG cells (3 of 4)

ABSTRACT: HepaRG cells were exposed in triplicate to three agrichemicals for 24hrs at 8 concentrations and a DMSO vehicle control (0.001, 0.003, 0.01, 0.03, 0.1, 0.3, 1, 3, and 10 μM plus DMSO vehicle controls). While a common set of DMSO controls was used, these CEL files were RMA normalized independently with each of the chemical treated groups. Gene expression was measured on an Affymetrix GeneTitan system. The compounds used were fenbuconazole (a.k.a FENB, CAS # 114369-43-6) a triazole fungicide, imazalil (a.k.a. IMAZ, CAS # 35554-44-0), an azole pesticide, and 2,4-dichlorophenoxyacetic acid (a.k.a. 2,4-D or 2-4-D in file names, CAS # 94-75-7), a chlorophenoxy herbicide.

ORGANISM(S): Homo sapiens

PROVIDER: GSE109511 | GEO | 2018/12/21

REPOSITORIES: GEO

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Real-time quantitative PCR analysis of fatty acid metabolism genes of liver tissue from wild-type and PPARα (-/-) mice exposed to 2,4-dinitrotoluene (fatty acid)

Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice.

2014-06-30 | GSE50168 | GEO

Real-time quantitative PCR analysis of fatty acid metabolism genes of liver tissue from wild-type and PPARα (-/-) mice exposed to 2,4-dinitrotoluene (glucose)

Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice.

2014-06-30 | GSE50169 | GEO

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