Ascorbic acid accumulation

Kostic, D. et al. (1995). Intestinal absorption, serum clearance, and interactions between lutein and beta-carotene when administered to human adults in separate or combined oral doses. Am. J. Clin. Nutr. 62 604—610. Kuo, S. M. et al. (2001). Dihydropyridine calcium channel blockers inhibit ascorbic acid accumulation in human intestinal Caco-2 cells. Life Sci. 68(15) 1751-1760. 

Adalid AM, Rosello S, Valcarcel M, Nuez F (2012) Analysis of the genetic control of beta-carotene and L-ascorbic acid accumulation in an orange-brownish wild cherry tomato accession. Euphytica 184 251-263... 

Welch, R. W., Bergsten, P. Butler, J. B., and Levine, M., 1993, Ascorbic acid accumulation and transport in human fibroblasts, Biochem. J. 294 505-510. 

The suggestion that there may be a sodium-dependent ascorbic acid transport mechanism in the pigmented layer of the ciliary epithelium (the layer which faces the blood side) fits well with a study conducted by Chu and Candia (1988), who isolated the rabbit iris-ciliary body and measured trans-tissue fluxes of labeled ascorbic acid. A net flux of ascorbic acid was observed in what would have been the blood-to-aqueous humor direction. Importantly, this net flux could be inhibited by phloridzin added to the blood side but not when added to the aqueous side. This finding is consistent with a model where active ascorbic acid is accumulated by the pigmented cells on the blood side of the ciliary epithelium bilayer, then passes via gap junctions into the nonpigmented cells, and finally diffuses into the aqueous humor. However, the situation may be more complex since cultured cells derived from the nonpigmented ciliary epithelium have also been shown to be capable of sodium-dependent ascorbic acid accumulation (Delamere et al., 1993). 

Washko, P., Rotrosen, D., and Levine, M., 1990, Ascorbic acid accumulation in plated human neutrophils, FEBS Lett. 260 101-104. 

Water-soluble vitamins removed by hemodialysis (HD) contribute to malnutrition and vitamin deficiency syndromes. Patients receiving HD often require replacement of water-soluble vitamins to prevent adverse effects. The vitamins that may require replacement are ascorbic acid, thiamine, biotin, folic acid, riboflavin, and pyridoxine. Patients receiving HD should receive a multivitamin B complex with vitamin C supplement, but should not take supplements that include fat-soluble vitamins, such as vitamins A, E, or K, which can accumulate in patients with renal failure. 

The feasibility of the above model rests on the formation of Cu(I) in the copper(II)-ascorbic acid system. A recent study firmly established that Cu(I) can indeed accumulate in the presence of a stabilizing ligand, Cl-, and in the absence of 02 (14). The actual form of the rate law is determined by the relative rates of Cu(I) formation and consumption, and further studies should clarify how the stability and reactivity of copper(I) are affected by the presence of various components and the conditions applied. 

Literature data on cytotoxic effects of photoexcited fullerene C60 are controversial. In the studies on transformed B-lymphocytes of Raji fine, phototoxic action of water-soluble carboxy-C60 was not revealed even upon its concentration of 5 x 10 5 M (Irie et al., 1996). In the study (Kamat et al., 2000) damaging effect of fullerenes C60 in dependence on intensity of irradiation toward CHO cells has been demonstrated. Using microsomal fraction of rat liver that was treated with C -cyclodextrin complex, it was shown that already in 5-30 min after UV-irradiation the accumulation of LPO products occurs that is suppressed by antioxidants like ascorbic acid and a-tocopherol. Similar effect of fullerenes C60 has been revealed in microsomal fraction of the cells of ascitic sarcoma 180 (Kamat et al., 2000). 

The biotransformation of low levels of fluorobenzene (ImM final concentration) to 4-fluorocatechol by whole cells of P. mendocina KRl (1.5 mg CDW/mL) is easy to reproduce. Under these conditions, 4-fluorocatechol is formed as a single product in the biotransformation after 120 min (Table 12.5). Biotransformations with P. mendocina KRl (1.5 mg CDW/mL) and higher concentrations of fluorobenzene (5mM final concentration) result in the formation of 4-fluorophenol (l.Smivi) as a major product. In addition, minor products, namely 2-fluorophenol, 3-fluorophenol, 4-fluorocatechol and 3-fluorocatechol, are also formed. In the presence of ascorbic acid, tyrosinase has the ability to convert 4-fluorophenol (1.8 him) to 4-fluorocatechol (1.3 mM). While this is a reproducible procedure, the 4-fluorocatechol does not accumulate as a single product (Table 12.5). 

Vitamins are chemically unrelated organic compounds that cannot be synthesized by humans and, therefore, must must be supplied by the diet. Nine vitamins (folic acid, cobalamin, ascorbic acid, pyridoxine, thiamine, niacin, riboflavin, biotin, and pantothenic acid) are classified as water-soluble, whereas four vitamins (vitamins A, D, K, and E) are termed fat-soluble (Figure 28.1). Vitamins are required to perform specific cellular functions, for example, many of the water-soluble vitamins are precursors of coenzymes for the enzymes of intermediary metabolism. In contrast to the water-soluble vitamins, only one fat soluble vitamin (vitamin K) has a coenzyme function. These vitamins are released, absorbed, and transported with the fat of the diet. They are not readily excreted in the urine, and significant quantities are stored in Die liver and adipose tissue. In fact, consumption of vitamins A and D in exoess of the recommended dietary allowances can lead to accumulation of toxic quantities of these compounds. 

King (1963) theorized that when the initial concentration of ascorbic acid increases beyond that necessary to saturate the copper in the system, the oxidation of ascorbic acid becomes so rapid and the products of the reaction accumulate so rapidly that they either block the reaction involving the lipids in the system or prevent the copper from acting as a catalyst. 

Whilst these acids are of minor importance in man, another multifunctional acid, ascorbic add (vitamin C 6), has an apparent role in human iron metabolism as one of the postulated factors aiding iron uptake. Ascorbic add reduces Fe111 to Fe" with probable complexation of the latter. It thus converts Fe"1 to a more soluble form. Ascorbic acid can also reduce Cu" to Cu1 (equation 1), and there is accumulating evidence of a link between the metabolism of ascorbic acid and that of Cu.34... 

Asai et al. (1999) determined that phospholipid hydroperoxides (PLOOH) are key products for oxidative injury in membranous phospholipid layers in the plasma, red blood cells (RBC), and liver of mice. The formation and accumulation of PLOOH have been confirmed in several cellular disorders, various diseases, and in aging. A lower PLOOH level was found in RBC of the spice-extract-fed mice (65 to 74% of the nonsupplemented control mice). The liver lipid peroxidizability induced with Fe2+/ascorbic acid was effectively suppressed in mice by dietary supplementation with the turmeric and capsicum extracts. Although no difference in the plasma lipids was observed, the liver triacylglycerol concentration of the turmeric-extract-fed mice was markedly reduced to half of the level in the control mice. These findings suggest that these spice extracts could act antioxidatively in vivo by food supplementation, and that the turmeric extract has the ability to prevent the deposition of triacylglycerols in the liver. 

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