Sulforaphane, a compound in broccoli, attaches to a specific receptor in human liver cells and reduces the activation of an enzyme that breaks down drugs and toxins.
Mechanism
Synthesis from 1 study
Sulforaphane locks onto a liver receptor that normally turns on a drug-metabolizing enzyme. When it's locked in, the receptor can't activate the gene for that enzyme, so the enzyme isn't made. Without enough enzyme, drugs are broken down more slowly.
Most probable mechanism
Sulforaphane attaches to a receptor in liver cells that normally turns on a drug-breaking enzyme. When sulforaphane is bound, the receptor cannot call in the helper proteins needed to start making the enzyme, so the enzyme is not produced, and drug breakdown slows down.
Sulforaphane binds directly to the ligand-binding domain of the steroid and xenobiotic receptor (SXR/hPXR)
Binding of sulforaphane prevents SXR/hPXR from recruiting coactivator proteins required for transcriptional activation
Failure to recruit coactivators suppresses transcription of the CYP3A4 gene
Reduced CYP3A4 gene expression leads to lower levels of CYP3A4 enzyme protein in liver cells
Decreased CYP3A4 enzyme concentration reduces the metabolic clearance of its substrate compounds
Evidence from Studies
Supporting (1)
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The Dietary Isothiocyanate Sulforaphane Is an Antagonist of the Human Steroid and Xenobiotic Nuclear Receptor
Contradicting (0)
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