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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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| TGF-β1 is one of three TGF-β ligands (β1, β2, β3) that initiate the TGF-β signaling cascade. In the context of cancer, TGF-β1 plays a dual role: Tumor Suppressor in Early Stages: In normal and early-stage tumor cells, TGF-β1 typically inhibits cell proliferation, induces apoptosis, and maintains tissue homeostasis. Tumor Promoter in Advanced Stages: As cancer progresses, TGF-β1 often promotes epithelial-to-mesenchymal transition (EMT), enhances invasiveness, contributes to immune evasion, and fosters a pro-metastatic microenvironment. Role in Early Tumorigenesis: Acts as a tumor suppressor via growth arrest and apoptosis. Role in Advanced Cancers: Promotes EMT, invasion, metastasis, and immune suppression. Expression in Cancer Types: Increased in advanced/ aggressive tumors in many cancer types. Prognostic Implications Elevated TGF-β1: associated with poor prognosis in several cancers due to its pro-tumorigenic functions. Therapeutic Targeting Blocking TGF-β1 activity (via antibodies or ligand traps) to reduce its tumor-promoting actions. |
| 4926- | PEITC, | PEITC inhibits the invasion and migration of colorectal cancer cells by blocking TGF-β-induced EMT |
| - | in-vitro, | CRC, | SW48 |
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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