Maintain mitochondria, the cells energy producer (ATP) and protector against damage from oxidative stress caused by reactive oxygen species and inflammatory proteins like cytokines.16 Acts as a cofactor for liver enzymes that metabolize and excrete xenobiotics, including drugs and heavy metals.17 Eliminates toxic substances like reactive oxygen species (ROS), free radicals, peroxides, and heavy metals.17 18 Maintain adequate levels of exogenous antioxidants vitamins C and E20,21,22 Supports DNA, protein, and cellular repair, aids immune and nerve function, transports amino acids, and promotes cell health and longevity.23 Regulates glutamate and GABA levels in the brain

We modeled the aging effects using the following data: expression fold changes of enzymes and transporters from the Tabula Muris Senis (TMS) dataset ( scaled initial concentrations of blood glucose, lactate, and -hydroxybutyrate according to the literature data on difference in their levels in aging (approximation, because effect size depends on the literature source) total NAD + and NADH concentration pool scaling (approximation), because it decreases in aging according to qualitative literature synaptic glutamate release pool (approximation, but synaptic input is set as the same for comparability of the results) scaling of reducing equivalents shuttles between cytosol and mitochondria: the NADH shuttle is a generalized rate equation based on the activity of multiple enzymes of malate-aspartate and glycerol-phosphate shuttles, for which we followed the literature to model it ( For the above factors, which mention approximative/approximation, the direction of change is according to the literature, but the absolute number of scaling factors (not known/contradictory in the literature) is set with an objective for the model to be steady at rest

doi: 10.1007/BF00400095 39 ZhangX.ZhaoY.ZhangM.PangX.XuJ.KangC.et al
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