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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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| Oxidative phosphorylation (or phosphorylation) is the fourth and final step in cellular respiration. Alterations in phosphorylation pathways result in serious outcomes in cancer. Many signalling pathways including Tyrosine kinase, MAP kinase, Cadherin-catenin complex, Cyclin-dependent kinase etc. are major players of the cell cycle and deregulation in their phosphorylation-dephosphorylation cascade has been shown to be manifested in the form of various types of cancers. Many tumors exhibit a well-known metabolic shift known as the Warburg effect, where glycolysis is favored over OxPhos even in the presence of oxygen. However, this is not universal. Many cancers, including certain subpopulations like cancer stem cells, still rely on OXPHOS for energy production, biosynthesis, and survival. – In several cancers, especially during metastasis or in tumors with high metabolic plasticity, OxPhos can remain active or even be upregulated to meet energy demands. In some cancers, high OxPhos activity correlates with aggressive features, resistance to standard therapies, and poor outcomes, particularly when tumor cells exploit mitochondrial metabolism for survival and metastasis. – Conversely, low OxPhos activity can be associated with a reliance on glycolysis, which is also linked with rapid tumor growth and certain adverse prognostic features. Inhibiting oxidative phosphorylation is not a universal strategy against all cancers. Targeting OXPHOS can potentially disrupt the metabolic flexibility of cancer cells, leading to their death or making them more susceptible to other treatments. Since normal cells also rely on OXPHOS, inhibitors must be carefully targeted to avoid significant toxicity to healthy tissues. Not all tumors are the same. Some may be more glycolytic, while others depend more on mitochondrial metabolism. Therefore, metabolic profiling of tumors is crucial before adopting this strategy. Inhibiting OXPHOS is being explored in combination with other treatments (such as chemo- or immunotherapies) to improve efficacy and overcome resistance. In cancer cells, metabolic reprogramming is a hallmark where cells often rely on glycolysis (known as the Warburg effect); however, many cancer types also depend on OXPHOS for energy production and survival. Targeting OXPHOS(using inhibitor) to increase the production of reactive oxygen species (ROS) can selectively induce oxidative stress and cell death in cancer cells. -One side effect of increased OXPHOS is the production of reactive oxygen species (ROS). -Many cancer cells therefore simultaneously upregulate antioxidant systems to mitigate the damaging effects of elevated ROS. -Increase in oxidative phosphorylation can inhibit cancer growth. |
| 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 |
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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