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| 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 |
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| Methylglyoxal (MGO) is a potent precursor of advanced glycosylation end-products (AGEs)
Glo1 catalyzes the conversion of cytotoxic MGO to nontoxic hemithioacetal using GSH as cofactor.
Because MGO rapidly forms hemithioacetal with GSH, elevated MGO will, in turn, deplete cellular GSH levels especially at low expression level of Glo2. Increased MGO, depletion of GSH and ATP are known to initiate apoptotic cell death. Some studies have investigated the potential of MGO as a therapeutic agent for cancer treatment. For example, MGO has been shown to: Enhance efficacy of chemotherapy and radiation therapy in certain types of cancer. Inhibit the growth of cancer stem cells. In terms of dietary sources, MGO is found in small amounts in various foods, including: Manuka honey, which is produced by bees that gather nectar from the manuka tree, apples and grapes, onions and garlic. In many cancers, elevated levels of methylglyoxal and its associated AGEs are often linked to poor prognosis. The accumulation of these compounds can lead to increased oxidative stress, inflammation, and disruption of cellular signaling pathways. Methylglyoxal is generally considered protumorigenic due to its role in promoting the formation of AGEs, which can lead to cellular damage, inflammation, and enhanced tumor growth. MG can also induce epithelial-to-mesenchymal transition (EMT), a process associated with increased metastatic potential. |
| 1892- | MGO, | Role of Glyoxalase 1 (Glo1) and methylglyoxal (MG) in behavior: recent advances and mechanistic insights |
| - | Review, | NA, | 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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