Serum ascorbic acid

A more recent study, which measured three established markers of free-radical activity in addition to serum ascorbic acid in two groups of elderly diabetic patients (with and without retinopathy), found no significant differences in any of the markers between patients and age-matched controls despite significant depletion of ascorbic acid in patients with diabetes, especially those with retinopathy (Sinclair et al., 1992). These rather paradoxical findings suggest the existence of a complex interrelationship between the levels of individual antioxidant molecules in cells and tissues. 

Ascorbic acid is a vitamin in primates. In most other animals, it can be synthesized by a branch of the glucoronic acid pathway (Chapter 18). It is apparently not changed into any coenzyme in the human being and participates as a vitamin in a reducing capacity in several biochemical reactions. These include the post-translational hydroxylation of proline in collagen biosynthesis (Chapter 8) and in tyrosine metabolism (Chapter 20). Ascorbic acid is oxidized to dehydroascorbic acid, a diketo derivative of ascorbate. Scurvy is a deficiency disease caused by a shortage of dietary ascorbic acid. In children, this results in defective bone formation in adults, extensive bleeding occurs in a number of locations. Scurvy is to be suspected if serum ascorbic acid levels fall below 1 jug/mL. 

The DNA adducts, deoxyadenosine and deoxygua-nosine, which are induced by malondialdehyde, the end-product of lipid peroxidation, accumulate in human breast tissues. These adducts are present at relatively higher concentrations in breast cancer cells compared to normal breast cells. In a recent study, serum antioxidative vitamin levels and lipid peroxidation were compared in gastric cancer patients. The level of serum ascorbic acid, a-tocopherol, p-carotene, and retinol were assessed. The levels of ascorbic acid in patients with gastric carcinoma were less than one-fifth of that in the control group, and the production of p-carotene and a-tocopherol were decreased, as well. 

Chronic intoxication with vitamin A has been reported to cause variously hypercalcemia, hyperglycae-mia, increased alkaline phosphatase, hypoproteinemia, hypoprothrombinemia, increased sulfobromphthalein retention, raised serum transaminases, low serum ascorbic acid, reduced protein content of the cerebrospinal fluid, raised urinary hydroxyproline, and hypercalciuria (SED-8, 800) (14). It is not always clear, however, whether these deviations are a cause or an effect of hypervitaminosis A. 

Blood and Animal Tissues. The most commonly used and practical procedure for evaluating vitamin C nutritional status is the measurement of serum (plasma) levels of ascorbic acid (87). Low plasma levels of ascorbic acid do not necessarily indicate scurvy, although scorbutic patients invariably have low or no plasma ascorbic acid, but continued low levels of plasma ascorbate of less than 0.10 mg/100 mL would eventually lead to signs and symptoms of scurvy. In general, serum ascorbic acid concentrations are usually more reflective of recent intakes rather than of total body stores (88). 

Recently, workers using serum ascorbic acid values as the reference of their estimation of ascorbic acid requirements in monkeys and baboons found that captivity and handling increased the ascorbic acid requirements (51,52). They concluded that captive monkeys required 20 mg of ascorbic acid/d in addition to fruit supplements. No differences were measured in the response of serum ascorbic acid after supplementations of 5 or 10 mg of ascorbic acid/kg of body weight/d in the baboon. 

Finally, elevated serum copper and ceruloplasmin blood levels were reported in schizophrenia (A6, All, B25), and it was postulated that this may be an important pathognomonic feature of this condition. Others, however, were unable to confirm this (Fll, H17, S21). It seems that the higher copper and ceruloplasmin levels reported earlier in schizophrenic individuals can be explained, partly on the basis of a high incidence of acute and chronic infection in institutionalized mentally ill individuals and partly by the presence of low serum ascorbic acid levels which may influence the particular type of oxidase activity determination used in one of these studies (A5). 

Simon, J.A., Hudes, E.S., and Tice, J.A. 2001. Relation of serum ascorbic acid to mortality among US adults. J. Am. Coll. Nutr. 20, 255-263. 

If histamine degradation is a physiological function of vitamin C, it is necessary to delineate the tissue level of ascorbic acid required for this effect. In the rat, which is capable of synthesizing ascorbic acid, serum ascorbic acid rose from 1.10 mg/100 ml to 1.63 mg/100 ml within 30 min of immobilization stress, nearly a 50% increase (Nakano and Suzuki, 1984). Liver ascorbate in these animals fell significantly after 15 min of stress, then rose dramatically to over 60% of the initial value within the next 15 min, indicating elevated hepatic biosynthesis of the vitamin. Adrenal ascorbic acid stores fell to 50% of the initial value following immobilization stress, and these levels remained depressed at 4 hr post-stress. Blood histamine levels rose 80%, from 38 to 68 ng/ml, peaking at about 30 min post-stress (Nakano and Suzuki, 1984). Hence, in the rat, stress induced a rapid rise in serum ascorbate which was fueled by ascorbic acid mobilized from tissue stores and by hepatic synthesis of ascorbate. 

Even passive smoking has been shown to increase experimental atherosclerosis (133). Exposure of healthy nonsmoking subjects to passive smoking, in a follow-up study, caused an acute decrease in serum ascorbic acid levels and antioxidant defense, decreased LDL capacity to resist oxidation, increased serum levels of lipid peroxidation end products, and LDL isolated from these subjects was taken up by cultured macrophages at an increased rate (134). Secondhand smoke also caused endothelial dysfunction and increased adrenergic responsiveness (which was abolished by inhibition of NOS and removal of endothelium) and atherosclerosis in hypercholesterolemic rabbits. These effects were mitigated by L-arginine supplementation (135). 

Supplementary ascorbic acid given to adults results in transient increases in plasma levels and increased excretion in the urine, with a degree of augmentation relating to dose, but not uniformly, in these substrates. Both leukocyte ascorbic acid (LAA) and serum ascorbic acid (SAA) are significantly elevated over unsupplemented levels at 1 g/day, rising proportionately to maximum uptakes, at about 6 g/day. It has been... 

The absorption of oral iron is decreased when tlie agent is administered with antacids, tetracyclines, penicillamine, and the fluoroquinolones. When iron is administered with levothyroxine, there may be a decrease in tlie effectiveness of levothyroxine When administered orally, iron deceases the absoqition of lev-odopa. Ascorbic acid increases tlie absoqition of oral iron. Iron dextran administered concurrently with chloramphenicol increases serum iron levels. 

FIGURE 4-18 Permselective coatings flow injection response of a poly(l,2-diaminoben-zene)-coated electrode to the following a, hydrogen peroxide (1 mM) b, ascorbic acid (1 mM) c, uric acid (1 mM) d, L-cysteine (1 mM) and e, control human serum. (Reproduced with permission from reference 63.)... 

There is evidence from a number of in vitro studies that the vitamin E peroxyl radical formed during fatty-acid degradation may be converted to vitamin E plus nonradical through the actions of vitamin C (Burton et al., 1985). RA patients have reduced serum ascorbate levels (Situnayake et al., 1991) and potentially a reduced capacity for the regeneration of vitamin E. In vitro studies suggest that vitamin E becomes a pro-oxidant when ascorbate levels are low (Bowry and Stocker, 1993). 

Lunec, J. and Blake, D.R, (1985). The determination of dehydroascorbic acid and ascorbic acid in the serum and synovial fluid of patients with rheumatoid arthritis. Free Rad. Res. Commun. 1, 31-39. 

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. 

Aminophthalate anion Atmospheric pressure active nitrogen Analyte pulse perturbation-chemiluminescence spectroscopy Arthromyces rasomus peroxidase Ascorbic acid Adenosine triphosphate Avalanche photodiode 5-Bromo-4-chloro-3-indolyl 2,6-Di-t< r/-bu(yl-4-mclhyl phenol Bioluminescence Polyoxyethylene (23) dodecanol Bovine serum albumin Critical micelle concentration Calf alkaline phosphatase Continuous-addition-of-reagent Continuous-addition-of-reagent chemiluminescence spectroscopy Catecholamines Catechol... 

The possible involvement of free radicals in the development of hypertension has been suspected for a long time. In 1988, Salonen et al. [73] demonstrated the marked elevation of blood pressure for persons with the lowest levels of plasma ascorbic acid and serum selenium concentrations. In subsequent studies these authors confirmed their first observations and showed that the supplementation with antioxidant combination of ascorbic acid, selenium, vitamin E, and carotene resulted in a significant decrease in diastonic blood pressure [74] and enhanced the resistance of atherogenic lipoproteins in human plasma to oxidative stress [75]. Kristal et al. [76] demonstrated that hypertention is accompanied by priming of PMNs although the enhancement of superoxide release was not correlated with the levels of blood pressure. Russo et al. [77] showed that essential hypertension patients are characterized by higher MDA levels and decreased SOD activities. 

Blood is transferred to test tubes and permitted to clot at room temperature for approximately 3 hours. The clot is removed by centrifugation and the serum saved for assay. Only serum was used it can be stored frozen with ascorbic acid added. 

Serum samples are prepared for assay by a modification of a previous method serum is used instead of whole blood (B18, T3). Serum is diluted 1 10 with buffer at pH 6.1 to which fresh 0.05% ascorbic acid has been added. To prepare buffer dissolve 27.8 g of NaH2P04 H20 in 1000 ml distilled water (Solution 1) dissolve 71.7 g Na2HP0412 H20... 

The presence of a certain number of amino acids is significant for the restitution of the immune system s cells, interferon synthesis process and other factors realization of the immune defense system. The decrease of full-form protein consumption is one of the causes of secondary immune-deficiency states. The significance of ascorbic acid presence for the immune system is supported by the fact that its concentration in the neutrophil granulocytes is 150 times higher than in the blood serum. The significance of retinol s and carotenoids role is supported in the cases of cell differentiation, where DNA synthesis increase, and proliferation decrease thus stabilizing the organism when under infection. 

Contraceptives (oral) and estrogens Ascorbic acid increases serum levels of estrogen and estrogen contained in oral contraceptives, possibly resulting in adverse reactions. 

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