ArticleBiochemical pharmacology2015
A metabolomic perspective of griseofulvin-induced liver injury in mice.
Article in Biochemical pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Development and characterization of a topical ferrochelatase inhibitor nanoemulsion for choroidal neovascularization therapy.International journal of pharmaceutics: X · 2026Article
- Dysbiosis in the Gut-Liver Axis Is Associated With Low Bone Mass During Murine Cholestasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Animal Models of Porphyria with Hepatic Involvement.Seminars in liver disease · 2025Review
- Roles of the ABCG2 Transporter in Protoporphyrin IX Distribution and Toxicity.Drug metabolism and disposition: the biological fate of chemicals · 2024Review
- Long-Acting Microparticle Formulation of Griseofulvin for Ocular Neovascularization Therapy.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
- Protoporphyrin IX-induced phototoxicity: Mechanisms and therapeutics.Pharmacology & therapeutics · 2023Review
- The assessment of the potential hepatotoxicity of new drugs byFrontiers in pharmacology · 2023Review
- Review
- Preparation and Evaluation of a Microsponge Dermal Stratum Corneum Retention Drug Delivery System for Griseofulvin.AAPS PharmSciTech · 2022Article
- Malaria parasite heme biosynthesis promotes and griseofulvin protects against cerebral malaria in mice.Nature communications · 2022Article
- Small-molecule inhibitors of ferrochelatase are antiangiogenic agents.Cell chemical biology · 2022Article
- Ferrochelatase regulates retinal neovascularization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Mitochondrial Heme Synthesis Enzymes as Therapeutic Targets in Vascular Diseases.Frontiers in pharmacology · 2020Article
- Development of Surface Molecularly Imprinted Polymers as Dispersive Solid Phase Extraction Coupled with HPLC Method for the Removal and Detection of Griseofulvin in Surface Water.International journal of environmental research and public health · 2019Article
- A metabolomic perspective of pazopanib-induced acute hepatotoxicity in mice.Xenobiotica; the fate of foreign compounds in biological systems · 2019Article
- Ferrochelatase is a therapeutic target for ocular neovascularization.EMBO molecular medicine · 2017Article
- Griseofulvin impairs intraerythrocytic growth of Plasmodium falciparum through ferrochelatase inhibition but lacks activity in an experimental human infection study.Scientific reports · 2017Article
- The Opportunities of Metabolomics in Drug Safety Evaluation.Current pharmacology reports · 2017Article
- Chronic Treatment with Isoniazid Causes Protoporphyrin IX Accumulation in Mouse Liver.Chemical research in toxicology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Griseofulvin (GSF) causes hepatic porphyria in mice, which mimics the liver injury associated with erythropoietic protoporphyria (EPP) in humans. The current study investigated the biochemical basis of GSF-induced liver injury in mice using a metabolimic approach. GSF treatment in mice resulted in significant accumulations of protoporphyrin IX (PPIX), N-methyl PPIX, bile acids, and glutathione (GSH) in the liver. Metabolomic analysis also revealed bioactivation pathways of GSF that contributed to the formation of GSF-PPIX, GSF-GSH and GSF-proline adducts. GSF-PPIX is the precursor of N-methyl PPIX. A six-fold increase of N-methyl PPIX was observed in the liver of mice after GSF treatment. N-methyl PPIX strongly inhibits ferrochelatase, the enzyme that converts PPIX to heme, and leads to PPIX accumulation. Excessive PPIX in the liver results in bile duct blockage and disturbs bile acid homeostasis. The accumulation of GSH in the liver was likely due to Nrf2-mediated upregulation of GSH synthesis. In summary, this study provides the biochemical basis of GSF-induced liver injury that can be used to understand the pathophysiology of EPP-associated liver injury in humans.
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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.