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| Phenethyl isothiocyanate (PEITC) is a naturally occurring small-molecule phytochemical best known for its role in cancer chemoprevention research. It belongs to the isothiocyanate class of organosulfur compounds and has the chemical formula C₉H₉NS. Source: Derived from glucosinolates in cruciferous vegetables PEITC in plants exists mainly as the glucosinolate precursor (gluconasturtiin). Upon tissue disruption (chewing, chopping), myrosinase converts gluconasturtiin → PEITC. -PEITC bioavailability from fresh, chopped microgreens is high -Co-consumption with other isothiocyanates is additive/synergistic -Peak plasma levels: ~1–3 hours post-consumption -Half-life: ~4–6 hours -Generally well tolerated up to 40 mg/day (mild GI irritation at higher dose) PEITC is best characterized for its dual role in xenobiotic metabolism: Inhibition of Phase I enzymes -Suppresses cytochrome P450 enzymes (e.g., CYP1A1, CYP2E1) -Reduces activation of pro-carcinogens -Selectively depletes GSH in cancer cells -Directly increases ROS beyond buffering capacity Key pathways in cancer cells -GSH depletion -Mitochondrial ROS amplification -ASK1/JNK apoptosis Chemo relevance -Frequently chemo-sensitizing -Opposite of NAC/GSH Induction of Phase II enzymes -Activates NRF2–KEAP1 signaling -Increases expression of detoxification and antioxidant enzymes such as: -Glutathione S-transferases (GSTs) -NAD(P)H quinone oxidoreductase 1 (NQO1) -Heme oxygenase-1 (HMOX1) In preclinical systems, PEITC has been shown to: -Deplete intracellular glutathione (GSH), increasing oxidative stress in cancer cells -Induce mitochondrial dysfunction and apoptosis -Inhibit histone deacetylases (HDACs) (context-dependent) -Suppress pro-survival signaling pathways (e.g., STAT3, NF-κB) -Target cancer stem–like cells in some models Dietary origins PEITC present in vegetables such as: -Watercress (the richest source) -Broccoli -Cabbage -Brussels sprouts -Radish Bioavailability depends on: -Food preparation -Gut microbiota (myrosinase activity if plant enzyme is inactive) watercress microgreens generally have higher PEITC (and/or its precursor gluconasturtiin) per gram than mature watercress. -The enrichment is most pronounced per unit fresh weight in the 7–14 day window. -Absolute values vary substantially with cultivar, light intensity, sulfur/nitrogen nutrition, and post-harvest handling. | Growth stage | Age | PEITC potential (mg / 100 g FW) | Relative | | --------------- | -------: | ------------------------------: | ---------------: | | **Microgreens** | 7–10 d | **3.0–6.0** | **~2–4×** mature | | **Microgreens** | 11–14 d | **2.5–5.0** | ~2–3× | | Baby leaf | 21–28 d | 1.5–3.0 | ~1–2× | | Mature leaf | 35–45+ d | 0.8–1.5 | baseline | Dry weight basis | Growth stage | PEITC potential (mg / g DW) | | --------------------- | --------------------------: | | Microgreens (7–10 d) | **1.8–3.5** | | Microgreens (11–14 d) | 1.5–3.0 | | Mature leaf | 0.6–1.2 | Expect 2–5× variability depending on: -Light spectrum (blue light ↑ glucosinolates) -Sulfur availability Practical optimization tips Lighting -12–16 h/day -150–300 µmol/m²/s PAR (typical shop LEDs at 20–30 cm distance) Soil -Peat or peat-blend preferred -Avoid over-watering (dilutes concentration) Nutrition (optional but effective) -One light watering with ¼-strength sulfate-containing fertilizer around day 4–5 can increase PEITC ~15–30% Harvest & use -Cut, rest 5–10 minutes, then consume (allows myrosinase to fully convert gluconasturtiin → PEITC) Dose: (100 g fresh microgreens ≈ 2–4 mg bioavailable PEITC) -ie below doses are not really acheivable from fresh microgreens Minimum biologically active dose (humans): ~10–15 mg PEITC/day Common efficacy range used in human trials: 20–40 mg/day Upper short-term doses studied (generally tolerated): 60 mg/day Diet-achievable with watercress microgreens: Yes, at realistic portions These doses are chemopreventive / pathway-modulating, not cytotoxic chemotherapy. | PEITC dose (mg/day) | Dominant biological effects | | ------------------: | ----------------------------------------------- | | **5–10 mg** | Phase II enzymes, mild NRF2 | | **10–20 mg** | HDAC inhibition, ROS signaling | | **20–40 mg** | Apoptosis, cell-cycle arrest, anti-inflammatory | | **40–60 mg** | Strong redox stress in cancer cells | | >60 mg | Limited data; GI irritation risk |
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| Type: pro-apoptotic protein |
| Bid is an abundant pro-apoptotic protein of the Bcl-2 family that is crucial for death receptor-mediated apoptosis in many cell systems. The expression of BID can serve as a prognostic marker in several cancers. Higher levels of BID are often associated with increased apoptosis and better treatment responses, while lower levels may indicate resistance to therapy and poorer outcomes. Generation of Truncated Bid (tBid): • When apoptosis is signaled, specific proteases (such as caspase-8) cleave full-length Bid into its truncated form, tBid. • tBid is the active form that translocates to mitochondria. So "the truncation of Bid" means that the protein has been converted into an active form (tBid) that supports apoptosis. |
| 4947- | PEITC, | Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G0/G1 Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death |
| - | in-vitro, | Oral, | HSC3 |
| 4923- | PEITC, | Quantitative chemical proteomics reveals that phenethyl isothiocyanate covalently targets BID to promote apoptosis |
| - | Study, | Var, | NA |
| 4940- | PEITC, | Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G 0/G 1 Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death |
| - | in-vitro, | Oral, | HSC3 |
| 4942- | PEITC, | Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G(0)/G(1) Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death |
| - | in-vitro, | Oral, | HSC3 |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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wNotes=0 sortOrder:rid,rpid