ArticleDrug metabolism and disposition: the biological fate of chemicals2016
A High Dose of Isoniazid Disturbs Endobiotic Homeostasis in Mouse Liver.
Article in Drug metabolism and disposition: the biological fate of chemicals, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Novel Thrice-Weekly Isoniazid plus Rifapentine Short-Course Regimen for the Treatment of Latent Tuberculosis Infection in a Murine Model.Infectious diseases & immunity · 2024Article
- System Biology Investigation Revealed Lipopolysaccharide and Alcohol-Induced Hepatocellular Carcinoma Resembled Hepatitis B Virus Immunobiology and Pathogenesis.International journal of molecular sciences · 2023Article
- New Histone Lysine Acylation Biomarkers and Their Roles in Epigenetic Regulation.Current protocols · 2023Article
- Bi-allelic hydroxymethylbilane synthase inactivation defines a homogenous clinico-molecular subtype of hepatocellular carcinoma.Journal of hepatology · 2022Article
- Isonicotinylation is a histone mark induced by the anti-tuberculosis first-line drug isoniazid.Nature communications · 2021Article
- Clinical perspectives of isoniazid-induced liver injury.Liver research (Beijing, China) · 2021Review
- Cell Type-Specific Roles of CD38 in the Interactions of Isoniazid with NADDrug metabolism and disposition: the biological fate of chemicals · 2020Article
- Isoniazid causes heart looping disorder in zebrafish embryos by the induction of oxidative stress.BMC pharmacology & toxicology · 2020Article
- The Multi-faceted Ecto-enzyme CD38: Roles in Immunomodulation, Cancer, Aging, and Metabolic Diseases.Frontiers in immunology · 2019Review
- Pharmacokinetics of Isoniazid-induced Rhabdomyolysis in a Girl.Internal medicine (Tokyo, Japan) · 2018Article
- CYP1A1 and 1B1-mediated metabolic pathways of dolutegravir, an HIV integrase inhibitor.Biochemical pharmacology · 2018Article
- Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury.Current pharmacology reports · 2018Article
- Deficiency of N-acetyltransferase increases the interactions of isoniazid with endobiotics in mouse liver.Biochemical pharmacology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Overdose of isoniazid (INH), an antituberculosis drug, can be life-threatening because of neurotoxicity. In clinical practice for management of INH overdose and acute toxicity, the potential of INH-induced hepatotoxicity is also considered. However, the biochemical basis of acute INH toxicity in the liver remains elusive. In the current study, we used an untargeted metabolomic approach to explore the acute effects of INH on endobiotic homeostasis in mouse liver. We found that overdose of INH resulted in accumulation of oleoyl-l-carnitine and linoleoyl-l-carnitine in the liver, indicating mitochondrial dysfunction. We also revealed the interactions between INH and fatty acyl-CoAs by identifying INH-fatty acid amides. In addition, we found that overdose of INH led to the accumulation of heme and oxidized NAD in the liver. We also identified an INH and NAD adduct in the liver. In this adduct, the nicotinamide moiety in NAD was replaced by INH. Furthermore, we illustrated that overdose of INH depleted vitamin B6 in the liver and blocked vitamin B6-dependent cystathionine degradation. These data suggest that INH interacts with multiple biochemical pathways in the liver during acute poisoning caused by INH overdose.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.