Methylene blue acts as an artificial electron carrier, promoting mitochondrial respiration. The net outcome is more energy available as ATP for cellular processes.[4]
Methylene blue supports mitochondrial respiration by functioning as an additional electron carrier[5]. MB receives electrons from NADH through mitochondrial complex I, itself being reduced to leuco-MB (MBH2). Leuco-MB then donates the electrons to cytochrome C, upon which it is recycled back to MB. These reactions serve to create a high proton (H+) concentration in the space between the inner & outer mitochondrial membranes. This leads to the passage of H+ down the concentration gradient, through mitochondrial complex V. In doing so, ADP & a phosphate (Pi) are joined to form ATP. Leuco-MB can also act as a free radical scavenger, neutralising superoxides by accepting electrons & itself becoming oxidized back to MB[6]. In this way, leuco-MB acts to prevent direct oxidative damage caused by free radicals.
Conversely, NR+ is ultimately cleaved to NAD+ and improves the NAD+/NADH ratio and is strictly adding to the availability of the pool of NAD+.
Obviously this says nothing about tissue specific preference of methylene blue vs. nicotinamide riboside, as enzymatic conversion of NR seems to be far greater in muscle tissue than perhaps the brain/nervous system while MB is lipophilic (for CNS preference). In other words, MB pretty much prefers nervous system tissue while NR prefers muscle tissue. Let's put that major issue aside for the moment.
I'm just wondering about the mechanism of action here and why methylene blue might be preferred over NR/NAM as a mitochondrial supporting supplement and what the trade-offs are.
Are we losing RNS/ROS signaling via methylene blue by shuttling activity strictly to complex IV and skipping I and III? Do we have data that show mitochondrial unfolded protein response (UPRmt) in methylene blue, levels of mnSOD, catalase, etc. ? such that we can see the difference with NR?
Edited by prophets, 31 August 2016 - 01:15 AM.
