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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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| Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases.
S, G1, G2, and M are the four phases of mitosis. |
| 4918- | PEITC, | Nutritional Sources and Anticancer Potential of Phenethyl Isothiocyanate: Molecular Mechanisms and Therapeutic Insights |
| - | Review, | Var, | NA |
| 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 |
| 4948- | PEITC, | Sensory acceptable equivalent doses of β-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo |
| - | vitro+vivo, | Oral, | CAL27 | - | vitro+vivo, | Oral, | FaDu | - | vitro+vivo, | Oral, | SCC4 | - | vitro+vivo, | Oral, | SCC9 |
| 4955- | PEITC, | Phenethyl isothiocyanate-induced cytoskeletal changes and cell death in lung cancer cells |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Lung, | H1299 |
| 4963- | PEITC, | Sensory Acceptable Equivalent Doses of β - Phenylethyl isothiocyanate (PEITC) Induce Cell Cycle Arrest and Retard Growth of p53 Mutated Oral Cancer In Vitro and In Vivo |
| - | vitro+vivo, | Oral, | CAL27 | - | vitro+vivo, | Oral, | FaDu | - | vitro+vivo, | Oral, | SCC4 | - | vitro+vivo, | Oral, | SCC9 |
| 5186- | PEITC, | Phenethyl Isothiocyanate inhibits STAT3 activation in prostate cancer cells |
| - | in-vitro, | Pca, | DU145 | - | in-vitro, | Pca, | LNCaP |
| 4919- | PEITC, | Natural compound PEITC inhibits gain of function of p53 mutants in cancer cells by switching YAP-binding partners between p53 and p73 |
| - | in-vitro, | Var, | NA |
| 4921- | PEITC, | The Potential Use of Phenethyl Isothiocyanate for Cancer Prevention |
| - | Review, | Var, | NA |
| - | Trial, | Oral, | NA |
| 4925- | PEITC, | PEITC triggers multiple forms of cell death by GSH-iron-ROS regulation in K7M2 murine osteosarcoma cells |
| - | in-vitro, | OS, | NA |
| 4929- | PEITC, | PacT, | Phenethyl isothiocyanate and paclitaxel synergistically enhanced apoptosis and alpha-tubulin hyperacetylation in breast cancer cells |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 |
| - | in-vitro, | Pca, | DU145 |
| 4932- | PEITC, | Pharmacokinetics and Pharmacodynamics of Phenethyl Isothiocyanate: Implications in Breast Cancer Prevention |
| - | Review, | BC, | NA |
| 4934- | PEITC, | Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 |
| 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 |
| 4944- | PEITC, | Phenethyl isothiocyanate induces DNA damage-associated G2/M arrest and subsequent apoptosis in oral cancer cells with varying p53 mutations |
| - | in-vitro, | Oral, | NA |
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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