tjohnson_nb wrote:Does this apply to RBCs, it seems to be talking about lymphocytes.
Referring to this excellent narrative https://allaboutblood.com/2013/08/06/er ... etabolism/
The Hexose Monophosphate Shunt:
Erythrocytes are subjected to a high degree of oxidative stress from exposure to drugs and chemicals and from oxygen transport... Glutathione is a tripeptide that scavenges reactive oxygen species and is oxidized in the process. Glutathione reductase regenerates glutathione by using NADPH as an electron donor. The only non-mitochondrial source of NADPH is the hexose monophosphate shunt...Normally about 10% of the glucose is metabolized through this shunt. When the erythrocyte is faced by an oxidizing stress almost 90% of the glucose may be metabolized through the shunt
Whether or not the mechanism of stimulating the hexose monophosphate shunt (aka pentose phosphate pathway or PPP) is the same in RBCs as in lymphocytes, I don't know. Whether or not the net overall effect is increased concentration
of glutathione as it is in lymphocytes, I don't know. I do know that DHAA has been demonstrated to induce NADPH production through the PPP via a number of mechanisms in many, many cell types and so this appears to be a general effect. Reported mechanisms have included inhibiting hexokinase, stimulation of the PPP enzymes G6PD, 6-phosphogluconate dehydrogenase, and transaldolase, and other mechanisms.
Douglas Q. Kitt, founder of ReCverin LLC, sellers of stabilized dehydroascorbic acid solutions.