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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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| – Some studies have reported upregulated expression of certain GABA receptor subunits (e.g., GABA_A receptor subunits) in breast tumors. – Increased expression has been associated with enhanced cell proliferation and migration, with some reports linking this to a poorer prognosis. -GABAergic transmission is deficient in anxiety. -Neurons expressing GABAA α1 receptors can mediate sedation, -while those expressing GABAA α2 receptors mediate anxiolytic. -In addition, extra-synaptic GABAA α5 receptors can also regulate the activity of hippocampal pyramidal cells, thereby affecting associative temporal and spatial memory Gamma-aminobutyric acid — Gamma-aminobutyric acid is an endogenous non-protein amino acid, inhibitory neurotransmitter, metabolic intermediate, and signaling ligand commonly abbreviated GABA. As a database target, it represents changes in GABA concentration, synthesis, secretion, uptake, extracellular accumulation, or GABA-shunt utilization rather than modulation of a specific GABA receptor. GABA is synthesized from glutamate by GAD1/GAD67 and GAD2/GAD65, transported by GABA transporters, and metabolized primarily by ABAT/GABA transaminase. In cancer, GABA may be produced by tumor, neural, stromal, or immune cells and can influence proliferation, invasion, mitochondrial metabolism, β-catenin signaling, and antitumor immunity. Its biological direction is strongly tumor-, receptor-, concentration-, and compartment-dependent. Typical cancer modulation: Variable/context-dependent. GABA production, secretion, extracellular accumulation, uptake, or GABA-shunt utilization may be ↑ in tumors that exploit GABA for metabolic adaptation, β-catenin activation, growth, invasion, or immune evasion. GABA signaling may instead suppress proliferation or migration in tumors expressing inhibitory GABA receptor configurations. Normal-cell relevance: GABA generally reduces neuronal excitability through GABA receptor signaling and also regulates pancreatic, immune, gastrointestinal, vascular, and endocrine functions. In Alzheimer’s disease, reduced phasic inhibition and excessive astrocyte-derived tonic GABA may coexist in different circuits; therefore total GABA direction alone may not indicate whether GABAergic function is beneficial or pathological. Target classification: Neurotransmitter; amino-acid metabolite; signaling ligand; tumor-microenvironment mediator; metabolic substrate. |
| 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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:123 Target#:1205 State#:% Dir#:2
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