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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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| Source: |
| Type: |
| NQO1 has attracted interest due to its roles in cell defense and marked inducibility during cellular stress. Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research. NQO1 (NAD(P)H:quinone oxidoreductase 1) is an enzyme that plays a significant role in cellular defense against oxidative stress and the metabolism of various compounds, including quinones and other electrophiles. Its function is crucial in protecting cells from damage caused by reactive oxygen species (ROS) and in the detoxification of potentially harmful substances. |
| 5014- | PEITC, | Xan, | Combination of xanthohumol and phenethyl isothiocyanate inhibits NF-κB and activates Nrf2 in pancreatic cancer cells |
| - | in-vitro, | PC, | NA |
| 5015- | Xan, | PEITC, | Comparison of the Impact of Xanthohumol and Phenethyl Isothiocyanate and Their Combination on Nrf2 and NF-κB Pathways in HepG2 Cells In Vitro and Tumor Burden In Vivo |
| - | in-vitro, | HCC, | HepG2 |
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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