ArticleXenobiotica; the fate of foreign compounds in biological systems2013
2,3,7,8-Tetrachlorodibenzo-p-dioxin enhances CCl4-induced hepatotoxicity in an aryl hydrocarbon receptor-dependent manner.
Article in Xenobiotica; the fate of foreign compounds in biological systems, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Circadian tryptophan metabolism contributes to systemic aryl hydrocarbon receptor activity.iScience · 2026Article
- Exploring transcriptomic databases to identify and experimentally validate tissue-specific consensus reference gene for gene expression normalization in BALB/c mice acutely exposed to 2,3,7,8-Tetrachlorodibenzo-Current research in toxicology · 2025Article
- Hypoxia Routes Tryptophan Homeostasis Towards Increased Tryptamine Production.Frontiers in immunology · 2021Article
- Dioxin Receptor Adjusts Liver Regeneration After Acute Toxic Injury and Protects Against Liver Carcinogenesis.Scientific reports · 2017Article
- 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) increases necroinflammation and hepatic stellate cell activation but does not exacerbate experimental liver fibrosis in mice.Toxicology and applied pharmacology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Cytochrome P4502E1 (CYP2E1) is involved in the biotransformation of several low molecular weight chemicals and plays an important role in the metabolic activation of carcinogens and hepatotoxins such as CCl(4). Induction of CYP2E1 is exerted mainly at posttranscriptional levels through mRNA and protein stabilization, and there is little evidence of xenobiotic induction at the transcriptional level. Previously, we reported microarray analysis data suggesting a decrease in Cyp2e1 gene expression on Ahr-null livers when compared to wild-type mouse livers. The goal of the present study was to determine whether 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased mouse CYP2E1 levels in an AhR-dependent manner and the impact on CCl(4)-induced hepatotoxicity. TCDD treatment induced CYP2E1 mRNA and protein levels in mouse liver, and this effect was aryl hydrocarbon receptor (AhR)-dependent. Moreover, TCDD pre-treatment increased the CCl(4)-induced alanine aminotransferase (ALT) activity, the extent of CCl(4)-induced necrosis, and the number of sinusoidal cells in wild-type animals, while this potentiating effect was not observed in Ahr-null mice. In conclusion, this study revealed that TCDD, probably in an AhR-dependent manner, exacerbated CCl(4)-induced hepatotoxicity through induction of CYP2E1.
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