Dehydroascorbic acid is the oxidised and reversible form of ascorbic acid or vitamin C. It can protect the brain and reduce stroke mortality, due to its ability to cross the blood-brain barrier, whereas vitamin C or ascorbic acid cannot easily do so. In one study it was proposed as a possible treatment for stroke victims (Huang 2001).
The reduced form or ascorbic acid reaches the interior of the cells via the sodium dependent vitamin C transporters (SVCTs). The body uses this "spent" form to deliver sufficient vitamin C to the interior of cells and mitochondria (which produce many free radicals) and to the brain (which has one of the highest concentrations of this vitamin) using the glucose transporters (GLUT1, GLUT10). Even in the midst of scurvy, the brain retains the last reserves of the vitamin to protect itself. In this form, it crosses the brain's protective barrier and reaches the interior of the mitochondria, where it is transformed back into ascorbic acid to fulfil its antioxidant function. Glutathione is primarily responsible for this final change in the whole organism. So is NADH, a form of vitamin B3 (Rivas 2008, Koshiishi 1998, Sebastian 2003, Verrax 2008).
Too much sugar in the diet makes it difficult for vitamin C to enter the brain. And the lack of glutathione and NADH in the Parkinson's patient hinders the mechanism of its recovery to the antioxidant form (redox mechanism).
Parkinson's patients often have 40 % of normal glutathione and, in advanced stages, only 2 %, which means that they are unable to restore dehydroascorbic acid to its active form, ascorbic acid. In addition, vitamin C protects the dopamine-producing areas from the oxidised remnants of the drug levodopa and the mitochondria, which generate a lot of oxidation in energy production. Without sufficient glutathione, this does not seem possible. Vitamin C regulates glutathione and glutathione restores its antioxidant capacity.
Under normal conditions, the active form of the vitamin is more than 95 % in human plasma and the oxidised form (DHA) is practically undetectable in most tissues (Rumsey, Levine 1998). It reaches higher concentrations when oxidative stress is present.
Dr. Katrin Mani (physician and professor of Molecular Medicine at Lund University, Sweden), commenting to the press on a study on Alzheimer's disease (Cheng 2011), left us with this observation that could be very important now and in the future:
"Another interesting finding is that useful vitamin C does not have to come from fresh fruit. In our experiments, we showed that vitamin C can also be absorbed in higher amounts in the form of dehydroascorbic acid from juice/juice that has been kept overnight in a refrigerator, for example".
One way to produce this oxidised form is to squeeze orange juice and leave the juice in the fridge overnight. By morning the ascorbic acid will have been oxidised, but not destroyed.
Sources:
Study: Fang Cheng, Roberto Cappai, G.D. Ciccotosto, Gabriel Svensson, Gerd Multhaup, Lars-Åke Fransson and Katrin Mani (2011). Suppression of amyloid beta A11-immunoreactivity by vitamin C: possible role of heparan sulfate oligosaccharides derived from glypican-1 by ascorbate-induced, NO-catalyzed degradation. Journal of Biological Chemistry.
researchgate.net/profile/Ka...
zeenews.india.com/news/heal...
Book: Jesús Márquez Rivera. La revolución de vitamina C, p. 47-48.
Article: Jesús Márquez Rivera. Vitamin C in the world of Parkinson's.