| Features: |
| Methylglyoxal is a reduced derivative of pyruvic acid that is produced by glycolysis and other metabolic pathways. It is involved in the formation of advanced glycation end products, DNA damage, and diabetes complications. -Methylglyoxal is specifically inhibits OXPHOS in cancer cells ? -Methylglyoxal in cancer cells inhibits GAPDH, an essential enzyme acting in the glycolsis pathway. GAPDH inhibition depletes ATP profoundly depriving the cancer cells of energy. -Activator of GABA A receptor Some research may indicate it can promote cancer growth. Dose: (30-40mg/day) 7.5mg/kg 4 times/day (plus 400mg Vit C) + VitB complex twice/day -Combine with curcumin(8g/d)? Combine with: Chitosan? Creatine (30-60 mins before) GLO1 inhibitors (Naringin, Curcumin) Nrf2 inhibitors: (ex Ascorbic Acid) GABA supplementation Metformin? Avoid combination with DCA? Pathways 1. Glyoxalase System Glyoxalase I and II: (glyoxalase system) which detoxifies methylglyoxal. In many cancers, the expression of glyoxalase I (and sometimes glyoxalase II) is upregulated. This allows tumor cells to tolerate higher MG levels resulting from their altered metabolism (often enhanced glycolysis), protecting them from dicarbonyl stress while simultaneously supporting their survival and proliferation. 2. Advanced Glycation End Products (AGEs) and RAGE Pathway AGE Formation:-Supplemented MG can increase the formation of advanced glycation end products (AGEs) RAGE Activation:AGEs can lead to the activation of RAGEE, which include the activation of NF-κB and MAPK pathways. 3. NF-κB Signaling Pathway: The activation of NF-κB by MG-induced AGE-RAGE signaling 4. MAPK Pathway: can be activated as a result of MG-induced oxidative and dicarbonyl stress . 5. ROS Generation and Oxidative Stress Methylglyoxal can raise intracellular ROS levels. (reinforcing the pro-tumorigenic environment.) -excessive ROS can be deleterious. Sources: Western or Chinese chemical suppliers under CAS number 78-98-8 |
| Source: |
| Type: |
| NADH is the reduced form of NAD⁺, meaning it has accepted electrons (and usually a proton) during metabolic reactions. When NAD⁺ accepts electrons (typically during metabolic processes like glycolysis, the citric acid cycle, and beta-oxidation), it becomes NADH. -By influencing the balance between NADH and NAD⁺, ENOX2 might shift the cellular redox state. An imbalance can lead to increased oxidative stress or changes in ROS signaling pathways. • The ratio between NADH and NAD⁺ is a key indicator of a cell’s metabolic state. • Some studies have suggested that abnormal NADH metabolism or shifts in the NADH/NAD⁺ ratio can be correlated with tumor aggressiveness or response to therapy. • For example, in certain cancers, a higher NADH/NAD⁺ ratio may be associated with more aggressive behavior, resistance to apoptosis, or poor prognosis. |
| 1891- | MGO, | Methylglyoxal induces mitochondria-dependent apoptosis in sarcoma |
| - | in-vitro, | SCC, | 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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:123 Target#:1120 State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid