Sulforaphane

Sulforaphane is a naturally occurring cancer chemopreventive compound belonging to the class of plant-derived products known as isothiocyanates. These bioactive molecules are abundant in cruciferous vegetables such as broccoli, cabbage, and arugula. Chemically, sulforaphane is also referred to as 4-methylsulfinylbutyl isothiocyanate, and it displays diverse biological activities, including antimicrobial, antioxidant, and anticancer effects.

Two major forms of sulforaphane are available: synthetic R,S-Sulforaphane (S111997 ≥95%, S140384 ≥70%, D424040 10mM in DMSO ), which has been shown to prevent mammary tumor development in animal models, and the naturally occurring, optically active R-Sulforaphane (R131741 ≥98%).

A central mechanism underlying sulforaphane’s anticancer properties is the induction of phase II detoxification enzymes, such as glutathione-S-transferase (GST) and quinone reductase (QR). Sulforaphane enhances the expression and activity of these enzymes, as well as γ-glutamyl-transpeptidase in lymphoblastoid and prostate cancer cells, leading to apoptosis and growth inhibition.

Sulforaphane has been shown to trigger apoptosis across multiple cancer cell lines:

• Colon carcinoma cells: Increases Bax expression, promotes cytochrome C release, and induces PARP cleavage, culminating in cell cycle arrest and apoptosis.

• Melanoma cells: Activates caspases, Bax, and p53, while reducing levels of Bcl-2, NF-κB, caspase-8, and Bid. These alterations promote apoptosis and inhibit proliferation.

Emerging evidence suggests that sulforaphane also exerts anticancer activity through epigenetic modulation. In colon cancer models, sulforaphane inhibits histone deacetylase (HDAC) activity and accelerates HDAC turnover. This process increases acetylation and degradation of DNA repair proteins, impairing the ability of cells to correct double-strand DNA breaks. The result is cell cycle arrest, autophagy, and apoptosis.

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