Non-psychotropic cannabinoids as inhibitors of TET1 protein
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
35462234
DOI
10.1016/j.bioorg.2022.105793
PII: S0045-2068(22)00198-5
Knihovny.cz E-zdroje
- Klíčová slova
- Cannabinoids, DNA methylation, Epigenetic, Iron chelation, TET1 protein,
- MeSH
- Cannabis * chemie MeSH
- kanabidiol * chemie farmakologie MeSH
- kanabinoidy * farmakologie MeSH
- kanabinol farmakologie MeSH
- simulace molekulového dockingu MeSH
- železnaté sloučeniny MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- kanabidiol * MeSH
- kanabinoidy * MeSH
- kanabinol MeSH
- železnaté sloučeniny MeSH
Non-psychotropic cannabinoids (e.g., cannabidiol, cannabinol and cannabigerol) are contained in numerous alimentary and medicinal products. Therefore, predicting and studying their possible side effects, such as changes in DNA methylation, is an important task for assessing the safety of these products. Interference with TET enzymes by chelating ferrous ions can contribute to the altered methylation pattern. All tested cannabinoids displayed a strong affinity for Fe(II) ions. Cannabidiol and cannabinol exhibited potent inhibitory activities (IC50 = 4.8 and 6.27 μM, respectively) towards the TET1 protein, whereas cannabigerol had no effect on the enzyme activity. An in silico molecular docking study revealed marked binding potential within the catalytic cavity for CBD/CBN, but some affinity was also found for CBG, thus the total lack of activity remains unexplained. These results imply that cannabinoids could affect the activity of the TET1 protein not only due to their affinity for Fe(II) but also due to other types of interactions (e.g., hydrophobic interactions and hydrogen bonding).
Citace poskytuje Crossref.org
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