ArticleFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association2012
Harmaline and harmalol inhibit the carcinogen-activating enzyme CYP1A1 via transcriptional and posttranslational mechanisms.
Article in Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 43 citations in OpenAlex.
- Targeting Chemical-induced Hepatocellular Carcinoma: Ameliorative Potential of Natural Compounds with Focus on Beta-carbolines.Mini reviews in medicinal chemistry · 2026Review
- Exploring the pharmacological potential of Lepionurus sylvestris blume: from folklore medicinal usage to modern drug development strategies using in vitro and in silico analyses.BMC complementary medicine and therapies · 2024Article
- Synthesis of fused polycyclic β-carboline derivatives using Ugi-4CR followed by cascade cyclization.Molecular diversity · 2023Article
- Photosensitizing properties and subcellular localisation of 3,4-dihydro-β-carbolines harmaline and harmalol.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023Article
- Antiviral activities of plant-derived indole and β-carboline alkaloids against human and avian influenza viruses.Scientific reports · 2023Article
- Chemoinformatic analysis of alkaloids isolated from Peganum genus.Molecular diversity · 2022Article
- Identifying Toxicologically Significant Compounds in Urban Wildfire Ash UsingEnvironmental science & technology · 2021Article
- Cytotoxic indole alkaloids against human leukemia cell lines from the toxic plant Peganum harmala.Toxins · 2015Article
- Synthesis and Fungicidal Activity of β-Carboline Alkaloids and Their Derivatives.Molecules (Basel, Switzerland) · 2015Article
- Article
- Pharmacological and therapeutic effects of Peganum harmala and its main alkaloids.Pharmacognosy reviews · 2013Review
- Harmine and harmaline downregulate TCDD-induced Cyp1a1 in the livers and lungs of C57BL/6 mice.BioMed research international · 2013Article
- Pharmacological and phytochemical appraisal of selected medicinal plants from jordan with claimed antidiabetic activities.Scientia pharmaceuticaReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Dioxins are known to cause several human cancers through activation of the aryl hydrocarbon receptor (AhR). Harmaline and harmalol are dihydro-β-carboline compounds present in several medicinal plants such as Peganum harmala. We have previously demonstrated the ability of P. harmala extract to inhibit TCDD-mediated induction of Cyp1a1 in murine hepatoma Hepa 1c1c7 cells. Therefore, the aim of this study is to examine the effect of harmaline and its main metabolite, harmalol, on dioxin-mediated induction of CYP1A1 in human hepatoma HepG2 cells. Our results showed that harmaline and harmalol at concentrations of (0.5-12.5μM) significantly inhibited the dioxin-induced CYP1A1 at mRNA, protein and activity levels in a concentration-dependent manner. The role of AhR was determined by the inhibition of the TCDD-mediated induction of AhR-dependent luciferase activity and the AhR/ARNT/XRE formation by both harmaline and harmalol. In addition, harmaline significantly displaced [(3)H]TCDD in the competitive ligand binding assay. At posttranslational level, both harmaline and harmalol decreased the protein stability of CYP1A1, suggesting that posttranslational modifications are involved. Moreover, the posttranslational modifications of harmaline and harmalol involve ubiquitin-proteasomal pathway and direct inhibitory effects of both compounds on CYP1A1 enzyme. These data suggest that harmaline and harmalol are promising agents for preventing dioxin-mediated effects.
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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.