"Lyposomal delivery is . . . energy-sparing. . . . "Similarly, liposomes can directly deliver active, reduced vitamin C directly into the cells. Most commonly, vitamin C must be in its oxidized (spent) form to penetrate the cell membrane. Cellular electron stores must then be tapped to convert the oxidized vitamin C back to its active form." (His parenthesis, and bold/italics.)
1. Why did biochemist/exert Sherry Lewin write in Vitamin C: Its Biology and Medical Potential that vitamin C traveled in the blood as ascorbic acid? (And as SA in the lymph?)
2. Why did Cathcart report that he could only achieve the 'ascorbate effect' orally, with ascorbic acid?
3. Why would vitamin C and glucose 'compete' for entry into cells? (Ely's GAA theory)
4. And I still don't understand how donating an electron "changes the molecule" so that it can use the GLUT receptor. Why couldn't AA use the GLUT receptor?
One scenario might be that "Free" AA does rapidly break down into DHA in the blood (that which doesn't attach to sodium) and this resulting DHA uses the GLUT transporters as reported. However, Sherry Lewin also notes that DHA is short-lived, and further breaks down quickly into substances that can not be recyled back into vitamin C.
Steve, is there an experiment that could be run in water to test the idea that "free" AA will combine with sodium, and verify how much, etc?
Steve Brown wrote:Considering that the uptake of vitamin C by cells is preferentially for dehydroascorbic acid raises two questions in my mind.
Steve Brown wrote:I prepared a solution of 210 mg of sodium bicarbonate in 100 ml of water at approximately 100 degrees Fahrenheit. Into that solution I sprinkled a few milligrams of ascorbic acid. It sank to the bottom of the beaker, and there was no apparent fizzing. I stirred it, and the ascorbic acid powder dissolved. Carbon dioxide may have been generated, in which case the gas was too diffuse to manifest as visible bubbles, going instead into solution.
uptake of vitamin C by cells is preferentially for dehydroascorbic acid
ofonorow wrote:Thank you for running this experiment.
And from this, what do you think we can conclude?
It would seem that you showed that ascorbic acid can be in the blood at the combination/concentrations found in the blood and not necessarily react with the sodium bicarbonate.
ofonorow wrote:Thank you for the help on the difference in molecules between AA and DHAA, but I still do not understand the often made statement "uptake of vitamin C by cells is preferentially for dehydroascorbic acid."
ofonorow wrote:...especially in light of that paper johnwen cited on ascorbate uptake by liver cells which doesn't even mention glucose uptake. In fact, while "sodium" dependent transporters are involved, the experimenters used ascorbic acid! I think your discussion above helps explain how SDVT work - with ascorbic acid - because of the NA+ ions in solution.
ofonorow wrote:So far the mechanism, in my mind, from this discussion is that your statement should be modified to
"the uptake of vitamin C by GLUT transporters in cells is preferentially for dehydroascorbic acid"
ofonorow wrote:...and from my reading of the other paper, I propose (for discussion) that
"the uptake of vitamin C by cells is preferentially for ascorbic acid from SDVT transporters"
ofonorow wrote:and this...
"The uptake of vitamin C in cells is preferentially ascorbic acid, but that vitamin C enter cells in its oxidized form as dehydroascorbic acid which competes with glucose"
ofonorow wrote:Getting late but the number of each kind of receptors on each kind of cell would be important.
ofonorow wrote:Recently doctor Levy pointed me to a paper that showed the number of GLUT on breast cancer cells was many times the number of healthy breast cells, indicating a strong preferential for DHAA by cancer cells. (Will post reference here later. The number of GLUT (insulin receptors) found in the cancer cells were about 12 times normal cells)
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