Johnwen wrote:DHA is the oxidized form of ascorbic acid.
Will it kill virus’s? Yes, Anaerobic varied types!
Will AA kill virus’s? Yes, Aerobic varied types!
Will it do a better Job then AA? No they both rely on the same transport mechanisms to get to the cells.
Pg 62. 2.4.5 Increased Membrane Permeability
It was concluded by several investigators (e.g. Martin, 1967, Hughs and Maton, 1968) that dehydroascorbic penetrates lipid membranes - such as those of erythrocytes - very much more than does ascorbate. The phenomenon has been attributed to the dehydroascorbic entity possessing a more lipid-like character than ascorbate. However, another way of viewing this phenomenon is to say that because dehydroascorbic possess a much greater power to reduce the interfacial tension, it can correspondingly increase membrane permeability. The implications of the respective formulations are not the same.
(i) An increased lipid-like character would help the DHA to enter the membrane from the aqeuous bulk, but having penetrated the membrane the DHA should prefer to stay in it because of the lipid character of the two. Hence, transfer of DHA from plasma into the inside of the cell would not be promoted, unless the contents of the cell were themselves more lipid-like than the plasma.
(ii) According to the previous explanations any ascorbate present with dehydroascorbic, outside the lipid membrane, need not penetrate the membrane any faster than when dehydroscorbic is absent. According to the view expressed here, the increased membrane permeability on contact with DHA should assist ascorbate penetration. Thus, in a solution containing a mixture of ascorbate and dehydroascorbic the permeability to AA should be higher than that when ascorbate alone is present.
AA and DHA can be viewed as antagonists, since their activities follow opposing directions. Further, AA, under physiological conditions, displays an ionic character, whereas DHA is more hydrophobic in character. Thus, at neutral pH values ....AA is an anion, while DHA is hardly ionized. Indeed the anhydrous form of DHA displays its relatively non-ionic character by being more lipid-soluble as indicated by the respective ...
ofonorow wrote:Backing up a little. Here is a quote from Sherry Lewin's 1976 book Vitamin C: Its Biology and Medical Potential. This was 1976 and I do not remember any discussion of "transporters" in this book! (What is a "transporter" anyway? Does it have atoms? A molecular structure?) Nor do I remember Linus Pauling discussing them much.
Ascorbic acid is absorbed in the body by both active transport and simple diffusion. Sodium-Dependent Active Transport—Sodium-Ascorbate Co-Transporters (SVCTs) and Hexose transporters (GLUTs)—are the two transporters required for absorption. SVCT1 and SVCT2 import the reduced form of ascorbate across plasma membrane. GLUT1 and GLUT3 are the two glucose transporters, and transfer only the dehydroascorbic acid form of Vitamin C. Although dehydroascorbic acid is absorbed in higher rate than ascorbate, the amount of dehydroascorbic acid found in plasma and tissues under normal conditions is low, as cells rapidly reduce dehydroascorbic acid to ascorbate. Thus, SVCTs appear to be the predominant system for vitamin C transport in the body.
SVCT2 is involved in vitamin C transport in almost every tissue, the notable exception being red blood cells, which lose SVCT proteins during maturation. "SVCT2 knockout" animals genetically engineered to lack this functional gene, die shortly after birth, suggesting that SVCT2-mediated vitamin C transport is necessary for life.
One that stood out to me was that in order to get DHA you need L-Ascorbic acid. The other form of V-C is D-erythroascorbic acid (D-ascorbic acid) will not turn yellow when oxidized and the reason it’s used as preservative in foods. The other thing with D-Ascorbic is it will not convert in the body to AA. However it is a excellent anti-oxidant but once it absorbs it’s oxygen molecules out the door it goes. If you want to reduce it! you need a yeast!
If you have yeasts in your body at the quantity needed to reverse it You got bigger problems.
When ingested, DHAA is absorbed and appears in the bloodstream (as reduced ascorbate) more quickly than when reduced ascorbate itself is ingested. The peak levels occurs somewhere around 30 to 90 minutes after ingestion. The peak blood level achieved by ingesting 5 grams DHAA was twice as high as the peak level achieved by the same individual when he ingested 5 grams of reduced ascorbate. More rapid uptake and higher intracellular levels from exposing cells to DHAA as opposed to reduced ascorbate has been demonstrated in many in vitro studies. This phenomenon is currently attributed to characteristics of the GLUT transporters.
Q: can we use color to test between L- and D- ascorbate?
A: No! Absolutely not. The color change occurs by reactions
in successive stages with oxygen. The right or left shape
of the molecular structure has no effect on this.
Q: why do some ascorbate solutions turn yellow quicker
A: This is a function of pH, temperature and duration.
Lower pH more acidic solutions are protected against
auto-oxidation as hydronium ions stick to and cover up
oxidizable electrons. Higher temperatures speed up collisions
with oxygen and accelerate the reaction rate. Older solutions
had more time to react and turn yellow.
ofonorow wrote:Begs the question, where did the electrons come from that "reduced" DHAA back to AA in the blood stream?
ofonorow wrote:This claim also makes me wonder how a blood test can distinguish between the reduced and oxidized form of vitamin C in the blood?
I participate in many forums and try to always be polite. I always live to regret when I fail to do so. I made a "snarky" comment previously. Please accept my apology, and my commitment to communicate with you with the respect you deserve as a well-read and intelligent person. I confess to taking the characterization of DHAA as "orange crap" in a personal way. I hope you understand that I have invested a huge part of my life in this molecule, and sometimes fail to remember that it is not one of my children!davea0511 wrote:But as Mr. Kitt seems concerned about my credentials...
It is a very common misconception. Thank you for giving me the opportunity to clarify it in this thread.davea0511 wrote:I've been wrong about a lot of things and one was thinking that the discoloration was DHA, and I think it must be a fairly common misconception...
Please note this statement from the cited study: "In drinking water samples, contaminated with copper from the pipes and buffered with bicarbonate, 35% of the added vitamin C was oxidized to dehydroascorbic acid within 15 min. After 3 h incubation at room temperature, 93% of the added (2 mM) ascorbic acid had been oxidized." 2mM is a quite dilute solution, 353 mg in one liter. According to this study, after 15 minutes, we could expect 123 mg of AA to be oxidized in the presence of copper ions and buffered with bicarbonate in one liter. Let's assume (incorrectly, as I will explain in a minute) that we recovered all 123 mg as DHAA. It appears that we could consume a 1 gram dose of DHAA by merely drinking about 8 liters, or almost 2 gallons. That's silly of course, but why wouldn't we just cut back on the amount of water? I mean, 353 mg of AA will easily dissolve in 100 mL of water which would be a lot easier to drink in one sitting. The reason is that more concentrated solutions of AA are much more stable to oxidation, even if the solution is made non-acidic and contains copper ions (both being conditions that greatly accelerate AA oxidation). But back to whether or not the product water actually contains very much DHAA:davea0511 wrote:...35% of AA becomes DHA within 15 minutes of being in tap water, due to mobility of Fe and Cu in that environment (plus added Fe and Cu in tap water) http://www.ncbi.nlm.nih.gov/pubmed/15493459 ...to suggest that DHA is complicated to create, requiring an enzyme from zucchini, that contradicts the study I just linked.
Actually, the tap-water study did say that: "The dehydroascorbic acid formed was further decomposed to oxalic acid and threonic acid by the hydrogen peroxide generated from the copper (I) autooxidation in the presence of oxygen." I don't have access to the full-text of this article, the statements I've quoted are from the abstract you supplied as a link. So I don't know the time frame within which the DHAA was "decomposed to oxalic acid and threonic acid" in their study. I also don't know what the actual pH of the solution "buffered with bicarbonate" was, but it isn't uncommon for this to mean neutral or physiological pH. I can cite a reference that says the half-life of DHAA in solution at physiological pH is about 7.5 minutes. So, you see, it is not at all "incredible" that most of the DHAA in that particular solution will become something else almost immediately...it is, in fact, rapidly becoming something else just about as fast as it is being formed. This is the dilemma of trying to create DHAA in useful quantity; the conditions that favor AA oxidation (e.g. non-acidic pH) generally favor DHAA degradation even more. So let me qualify my contention, as you have stated it, that DHAA is complicated to create; it is complicated to create in sufficient quantity and stability for dietary or topical use.davea0511 wrote:Is he saying that actually after 15 minute 35% of the AA is neither AA or DHA because that DHA immediately became something else - because that's incredible. Why didn't the tap-water study say that?
Dear Dr. Ginter,
A recent article states that dehydroascorbic acid (DHAA) is a form of vitamin C.
Our question, can you give DHAA to guinea pigs and keep them alive?
Vitamin C Foundation.org
Yes, you could do it.
Sincerely, Emil Ginter
Users browsing this forum: No registered users and 1 guest