Ascorbic accumulation

Nardai G, Braun L, Csala M, Mile V, Csermely P, Benedetti A, Mandl J, Banhegyi G. Protein-disulfide isomerase- and protein thiol-dependent dehydroascorbate reduction and ascorbate accumulation in the lumen of the endoplasmic reticulum. J. Biol. Chem. 2001 276 8825-8828. 

Korcok, J. Dixon, S. J. Lo, T. C. Y. Wilson, J. X. 2003. Differential effects of glucose on debydroascorbic acid transport and intracellular ascorbate accumulation in astrocytes and skeletal myocytes. Brain Res. 993 201-207. 

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. 

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. 

II. Ascorbate Peroxidase (EC 1.11.1.11) APX isoenzyme, plays an important role in the metabolism of H202 in higher plants. APX utilizes Ascorbate (Asx) as its specific electron donor to reduce H202 to water with the generation of monodehydroascorbate, involved in the Ascorbate-GSH cycle. Thus, APX in combination with the effective Asx-GSH cycle functions to prevent the accumulation of toxic levels of H202. 

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... 

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