Ascorbic acid active transport

Vitamin C Ascorbic acid is the most important redox substance of cell metabolism. The body content probably amounts to about 2-5 g, the major part being stored in the liver and muscles. Intestinal absorption (80-90%) is an active, sodium-dependent process. The transport of ascorbic acid in the blood probably takes place as an ascorbic acid-albumin complex. Cellular uptake is stimulated by insulin. 

Equations 2 and 3 are valid if there are no active transport and/or other complicated transfer processes. Neglecting partitioning due to pH diflFerences in various tissues, the concentration of unbound ascorbic acid is assumed to be equal in all volumes into which the compound is distributed. Applying this principle to a single tissue. Equation 4 can be derived easily ... 

Different concentrations in compartments that can exchange ascorbic acid may also be achieved by nonlinear transfers such as active transport processes. Nonlinearity, however, cannot be determined by experimental designs using only one steady state level. The brain, adrenals, pituitary gland, and eyes take up ascorbic acid by an energy-dependent active transport mechanism (30,31). 

Absorption of ascorbic acid in the gut is a passive process for the rat (18), while scurvy-prone animals require an active transport system with a Na -dependent, gradient-coupled carrier mechanism that is inhibited by ouabain (19,20). A transport model is favored that fea-... 

In humans there is a Na -dependent active transport system with a Km of about 1 mM. Absorption is very eflBcient at low intakes of ascorbic acid and becomes poor as stomach levels of ascorbic acid increase. The upper level of ascorbic acid in the blood is limited by kidney clearance with Tm of 1.5 mg/100 mL. Where intestinal absorption is excessive the eflSciency of the kidney clearance improves. Transfer of ascorbic acid into the central nervous system and other tissues is a facilitated saturable process. Therefore, control at all levels appears to sharply limit maximum levels of ascorbate in tissues. 

Uptake. Ascorbic acid is absorbed from the intestine by a sodium-dependent active transport system that is saturable. As the concentration of vitamin C increases in the intestinal tract, the absorption changes to passive diffusion. Once in systemic circulation, there are specific transporters based on cell types. 

The concentration of ascorbate in the human plasma is 25 pM and above. Cells take up ascorbate by a Na -coupled uptake mechanism against a concentration gradient. A marked stereo-selectivity for L-ascorbic acid relative to D-isoascorbic acid in their cellular transport has been shown by Franceschi et al. [12]. The same transport is also important in the intestine. The nutritional supply of ascorbic acid is the only source for this vitamin in humans, primates, and guinea pigs. Other mammals are able to produce ascorbic acid. There exists sufficient evidence for an active role of ascorbate as an antioxidant in vivo. Decreased ascorbic acid will increase lipid peroxidation and decrease vitamin E and is connected with oxidative DNA damage. The supply of ascorbate in some cases will reduce the amount of oxidative damage in diseases that... 

In the 1960s, Mitchell showed how the energy released in electron transport is used to pump protons from the matrix side of the inner mitochondrial membrane to the cytoplasm side. The subsequent dissipation of the proton gradient, via gates in the stalks of the knoblike projections of the inner membrane, activate ATP synthetase. Recently ascorbic acid has been implicated in such membrane potentiation by the establishment of proton gradients in the plasma membrane vesicles extracted from the soybean (Glycine max). 

While ascorbate is transported into isolated intact chloroplasts (Anderson et al., 1983b Beck et al., 1983 Foyer and Lelandais, 1996), the thylakoid membranes appear to have no carrier system to transport ascorbate into the thylakoid lumen (Foyer and Lelandais, 1996). This is surprising since the enzyme VDE, located inside the thylakoid, requires ascorbate to convert violaxanthin to zeaxanthin (Fig. 2). Upon illumination the pH ofthe lumen falls and VDE binds to the lumenal side of the thylakoid membrane and becomes active (Hager and Holocher, 1994 Rockholmand Yamamoto, 1996). The affinity of VDE for ascorbate is strongly dependent on pH, because ascorbic acid is the true substrate of the enzyme (Bratt et al., 1995). The addition ofHjOj to illuminated thylakoid membrane preparations induces a transient inhibition of zeaxanthin formation (Neubauer and Yamamoto, 1992), suggesting competition for ascorbate between the Mehler-peroxidase cycle and the VDE reaction. Since the ascorbate pool in the chloroplast stroma is substantial (10-50 rnM), sufficient amounts of ascorbic acid may be able to aoss the membrane by diffusion (Eoyer et al., 1983 Foyer, 1993 Foyer and Lelandais,... 

Ascorbic acid deficiency also reduces the activity of several dehydrogenases involved in the Krebs cycle. The mechanism by which the vitamin leads to such alteration is not clear, but the effect is reversed by insulin administration. Thus, miscellaneous observations on the effect of ascorbic acid on carbohydrate metabolism have been made, but they are difficult to interpret because no specific coenzyme effect of ascorbic acid has been demonstrated. Again, ascorbic acid is assumed to be directly involved in an electron transport chain that involves cytochrome and NAD. The vitamin may also affect the electron transport chain indirectly because a decrease in NADH concentration has been observed in vitamin C deficiency. But this decrease may also result from an interference with the insulin production because it is... 

Vitamin C and Ion attachment mass spectrometry with a temperature-pro-grarmned direct probe allows the detection of irrtact pyrolysis products. It, therefore, offers the opportunity to monitor directly thermal byproducts on a real-time basis and potentially to detect thermally imstable products. EGA-IAMS is used to study the real-time, non-isothermal decomposition of vitamin C [30]. The results were compared with those obtained in a similar study on thermal decomposition of vitamin C using pyrolysis GC/MS. Significant differences were found between the two techniques, in terms of the nature and relative amoimts of products formed. A major difference between the two techniques was in the transportation time of the pyrolysis products out of the pyrolysis chamber (or hot zone). The time was significantly shorter in EGA-IAMS than in pyrolysis GC/MS, which reduces the occmrcnce of secondary reactions of the primary pyrolysis products. Some decomposition products formed in the EGA-IAMS system were not detected in the previous pyrolysis GC/MS study [38] and thus were detected for the first time. For instance, dehydro-L-ascorbic acid was observed as a decomposition product. This compoimd was the main degradation product detected by means of EGA-IAMS. While it is an important compoimd because it possesses some biological activity, dehydro-L-ascotbic acid is difficult to measure due to its chemical instabihty. 

The ingested amounts of vitamin C are mainly absorbed in the duodenum, in the proximal jejunum, and through the buccal mucous membrane. The physiological daily intake of vitamin C of up to 180 mg is absorbed 80 to 90%. In humans and guinea pigs the absorption mechanism of L-ascorbate depends on a pH-dependent saturable active transport and relies on the presence of a carrier and sodium ions. Dehydroascorbic acid is absorbed by facilitated diffusion. For animals with the... 

Contrary to the active carrier-mediated transport of ascorbic acid into the cell, the intracellular transport into organelles like mitochondria follows carrier-free diffusion of both ascorbic acid and dehydroascorbic acid. Intramitochondrial dehydroascorbic acid is not reduced to ascorbic acid (Ingebretsen et al., 1982). 

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