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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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| The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues. Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance Factors that affect selectivity: 1. Ability of Cancer cells to preferentially absorb a product/drug -EPR-enhanced permeability and retention of cancer cells -nanoparticle formations/carriers may target cancer cells over normal cells -Liposomal formations. Also negatively/positively charged affects absorbtion 2. Product/drug effect may be different for normal vs cancer cells - hypoxia - transition metal content levels (iron/copper) change probability of fenton reaction. - pH levels - antiOxidant levels and defense levels 3. Bio-availability |
| 4949- | PEITC, | Phenethyl Isothiocyanate Exposure Promotes Oxidative Stress and Suppresses Sp1 Transcription Factor in Cancer Stem Cells |
| - | in-vitro, | Cerv, | HeLa |
| 4951- | PEITC, | ROS accumulation by PEITC selectively kills ovarian cancer cells via UPR-mediated apoptosis |
| - | in-vitro, | Ovarian, | PA1 | - | in-vitro, | Ovarian, | SKOV3 |
| 4954- | PEITC, | Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by β-phenylethyl isothiocyanate |
| - | vitro+vivo, | Ovarian, | SKOV3 |
| 4946- | PEITC, | Phenethyl Isothiocyanate Inhibits Oxidative Phosphorylation to Trigger Reactive Oxygen Species-mediated Death of Human Prostate Cancer Cells |
| - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | PC3 |
| 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 |
| 5183- | PEITC, | Cisplatin, | Phenethyl Isothiocyanate Induces Apoptosis Through ROS Generation and Caspase-3 Activation in Cervical Cancer Cells |
| - | in-vitro, | Cerv, | HeLa | - | in-vitro, | Nor, | HaCaT |
| 4922- | PEITC, | Phenethyl Isothiocyanate: A comprehensive review of anti-cancer mechanisms |
| - | Review, | Var, | NA |
| - | Trial, | Oral, | NA |
| 4928- | PEITC, | Dietary phytochemical PEITC restricts tumor development via modulation of epigenetic writers and erasers |
| - | vitro+vivo, | Colon, | SW-620 |
| 4941- | PEITC, | PEITC: A resounding molecule averts metastasis in breast cancer cells in vitro by regulating PKCδ/Aurora A interplay |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 |
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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