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Affect of liver transcriptome by acute acetaminophen exposure [miRNA]

ABSTRACT: To study the global changes of liver transcriptome after acetaminophen overdose. To study the global changes of transcriptome in the liver after acetaminophen overdose. Eight week old female C57BL/6 mice were fasted for 24 hours prior to a single intraperitoneal injection of 350mg/kg of acetaminophen in phosphate buffer saline (PBS) (treatment group) or PBS (control group). The mice were euthanized at different time points post exposure; plasma and tissue samples were collected for pathological examination and biochemical analyses.

ORGANISM(S): Mus musculus

SUBMITTER: Ji-Hoon Cho

PROVIDER: E-GEOD-42181 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The spectrum of circulating RNA: a window into systems toxicology.

Wang Kai K Yuan Yue Y Li Hong H Cho Ji-Hoon JH Huang David D Gray Li L Qin Shizhen S Galas David J DJ

Toxicological sciences : an official journal of the Society of Toxicology 20130128 2

Adverse effects caused by therapeutic drugs are a serious and costly health concern. Despite the body's systemic responses to therapeutics, the liver is often the focus of damage and is usually the focus of studies of toxic effects due to its active roles in the metabolism of xenobiotics. It is extremely difficult, however, to assess systemic responses with currently available methods. Comprehensive cataloging of cell-free circulating RNAs using next-generation sequencing technology may open a w ...[more]

PMID: 23358195

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Affect of liver transcriptome by acute acetaminophen exposure [mRNA]

Project description:To study the global changes of liver transcriptome after acetaminophen overdose. To study the global changes of transcriptome in the liver after acetaminophen overdose. Eight week old female C57BL/6 mice were fasted for 24 hours prior to a single intraperitoneal injection of 350mg/kg of acetaminophen in phosphate buffer saline (PBS) (treatment group) or PBS (control group). The mice were euthanized at different time points post exposure; plasma and tissue samples were collected for pathological examination and biochemical analyses.

2013-05-03 | E-GEOD-42178 | biostudies-arrayexpress

Affect of liver transcriptome by acute acetaminophen exposure

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-05-03 | E-GEOD-42182 | biostudies-arrayexpress

Transcription profiling of mouse liver after Acetaminophen intoxication

Project description:Acetaminophen (APAP) is the most widely used analgesic in the United States. Its acute overdose causes liver damage by inducing localized centrilobular cell death. Because of widespread use, APAP toxicity has become the most frequent cause of acute liver failure. Many factors have been associated with the susceptibility of APAP-induced liver injuries, however, few of them have been confirmed and used in the clinical setting. We tried to identify the subset of factors that could affect susceptibility to APAP-induced liver injury by an integrative genetic, transcriptional and 2-D-NMR-based metabolomic analysis across a panel of inbred mouse strains. Experiment Overall Design: After a single administration of high dose (300 mg/kg i.p.) APAP, liver and blood samples were extracted from 3 sensitive (C57B6, DBA/2, and SmJ) and 1 resistant (SJL) mice strains at 0, 3 and 6 hour after APAP exposure. Endogenous metabolites from liver samples were analyzed by 1H-13C 2-dimensional-NMR and gene expression changes occurring within these liver samples were simultaneously analyzed using Affymetrix microarrays. The transcriptional and metabolomic data was jointly analyzed, and functional information within the Gene Ontology database was used to identify the subset of genes that could affect susceptibility to APAP-induced liver injury in the early phase response.

2009-08-23 | E-GEOD-17649 | biostudies-arrayexpress

Hepatic responses of mice and rats to equivalent acetaminophen (APAP) insult – SWATH proteomics

Project description:The well-known difference in sensitivity of mice and rats to acetaminophen (APAP) liver injury has been related to differences in the fraction that is bioactivated to the reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI). Physiologically-based pharmacokinetic modelling was used to identify doses of APAP (300 and 1000 mg/kg in mice and rats, respectively) yielding similar hepatic burdens of NAPQI, to enable the comparison of temporal liver tissue responses under conditions of equivalent chemical insult.

2023-08-31 | PXD034438 | Pride

Modulation of the transcriptional response to recombinant IFN-Î² by Acetaminophen

Project description:We examined the effect of acetaminophen (APAP) on the transcriptional response induced by interferon-Î² (IFN-Î²). Transcript levels from total RNA isolated rom murine livers were determined using G4121B whole genome arrays. Keywords: Pharmakinetics, drug treatment 6-8 week male CD-1 mice were administered vehicle alone, APAP, IFN-Î² or IFN-Î² + APAP (n=5 per treatment per time point 40 animals total) and were euthanized at 1.5 or 4 hours post-treatment. Agilent 22k whole genome arrays were used to measure changes in mRNA transcripts in the liver mRNA. Stratatagene Universal Mouse RNA was used as a reference.

2010-10-18 | E-GEOD-18949 | biostudies-arrayexpress

Affect of liver transcriptome by acute acetaminophen exposure [miRNA]

Project description:To study the global changes of liver transcriptome after acetaminophen overdose.

2013-05-03 | GSE42181 | GEO

Affect of liver transcriptome by acute acetaminophen exposure [mRNA]

Project description:To study the global changes of liver transcriptome after acetaminophen overdose.

2013-05-03 | GSE42178 | GEO

Blood Gene Expression Profiling of an Early Acetaminophen Response (I)

Project description:Acetaminophen can adversely affect the liver especially when overdosed. We used whole blood as a surrogate to identify genes as potential early indicators of an acetaminophen-induced response. In a clinical study, healthy human subjects were dosed daily with 4g of either acetaminophen or placebo pills for 7 days and evaluated over the course of 14 days. Alanine aminotransferase (ALT) levels for responders to acetaminophen increased between days 4 and 9 after dosing and 12 genes were detected with expression profiles significantly altered within 24hrs. The early responsive genes separated the subjects by class and dose period. In addition, the genes clustered patients who overdosed on acetaminophen apart from controls and also predicted the exposure classifications with 100% accuracy. The responsive genes serve as early indicators of an acetaminophen exposure and their gene expression profiles can potentially be evaluated as molecular indicators for further consideration. Randomized, single-blind, placebo-controlled, clinical study. Healthy male and female individuals from 18 â 58 years old weighing 55 kg to 85 kg volunteered as subjects in the study. Subjects were enrolled for 14 days each and were acclimated for 3 days on a controlled, standardized whole-food diet in order to assure a uniform nutritional intake. Starting on day 0 and until day 7 relative to the start of dosing, each subject received daily repeat dosing every 6 hrs (i.e. 4x daily) of either 1g of acetaminophen or placebo pills orally. Blood was collected at 8 a.m. on each day of the clinical study for alanine aminotransferase (ALT) measurement and complete blood counts (CBC).

2016-02-16 | E-GEOD-70784 | biostudies-arrayexpress

Novel Protective Role of Nicotinamide Phosphoribosyltransferase in Acetaminophen-induced Acute Liver Injury in Mice

Project description:Acetaminophen overdose is the most common cause of acute liver injury (ALI) or acute liver failure in the USA. Its pathogenetic mechanisms are incompletely understood. Additional studies are warranted to identify new genetic risk factors for more mechanistic insights and new therapeutic target discoveries. The objective of this study was to explore the role and mechanisms of nicotinamide phosphoribosyltransferase (NAMPT) in acetaminophen-induced ALI. C57BL/6 Nampt gene wild type (Nampt+/+)-, heterozygous knockout (Nampt+/-)-, and overexpression (NamptOE)-mice were treated with overdose of acetaminophen, followed by histological, biochemical, and transcriptomic evaluation of liver injury. The mechanism of Nampt in acetaminophen -induced hepatocytic toxicity was also explored in cultured primary hepatocytes. Three lines of evidence have convergently demonstrated that acetaminophen overdose triggers the most severe oxidative stress and necrosis, and the highest expression of key necrosis driving genes in Nampt+/- mice, while the effects in NamptOE mice were least severe relative to Nampt+/+ mice. These findings support that NAMPT protects against acetaminophen induced ALI.

2018-04-03 | GSE110787 | GEO

Shifted Metabolic Bias in Livers of Mice Lacking Hepatocytic Thioredoxin Reductase-1 Protects Against Acetaminophen Toxicity

Project description:Genetic disruption of thioredoxin reductase 1 protects against acetaminophen (APAP) toxicity. To determine the role of the thioredoxin system on xenobiotic metabolism we challeneged wildtype and txnrd1liver-null mice with acetaminophen. Adult male wildtype and txnrd1 liver-null mice (C57BL6/J) were treated with either saline (PBS) or 100mg/kg APAP. Liver RNA was harvested eight hours after challenge and processed for microarray analysis. Comparison of 2 treatment conditions in 2 genotypes, biological replicates in triplicate.

2013-06-08 | E-GEOD-37874 | biostudies-arrayexpress

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