ArticleMolecular and cellular biochemistry2014
Lack of liver injury in Wistar rats treated with the combination of isoniazid and rifampicin.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Involvement of histone hypoacetylation in INH-induced rat liver injury.Toxicology research · 2018Article
- Isoniazid metabolism and hepatotoxicity.Acta pharmaceutica Sinica. B · 2016Review
- Mechanism of isoniazid-induced hepatotoxicity: then and now.British journal of clinical pharmacology · 2016Review
- Characterization of Conserved Toxicogenomic Responses in Chemically Exposed Hepatocytes across Species and Platforms.Environmental health perspectives · 2016Article
- D-penicillamine-induced granulomatous hepatitis in brown Norway rats.Molecular and cellular biochemistry · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Isoniazid (INH) can cause serious idiosyncratic liver injury. An animal model would greatly facilitate mechanistic studies, but it is essential that the mechanism in the model be similar to the liver injury that can occur in humans. We attempted to replicate a previous study in which Wistar rats treated with INH and rifampicin (RMP) developed liver injury, which was promising because of its delayed onset similar to the liver injury that can occur in humans. Wistar rats were treated with either a high dose of INH (150 mg/kg/day) or a combination of INH and RMP (75 mg/kg/day and 50 mg/kg/day, respectively) for up to 4 weeks. However, we did not observe any liver injury or evidence of an inflammatory infiltrate as had been reported; rather, we observed an increase in CTLA4-positive cells in the cervical lymph nodes as well as a decrease in serum CXCL1 and MCP-1. In short, we were unable to reproduce a previously reported model of delayed onset INH-induced liver injury in Wistar rats.
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Registered trials
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