Blood ascorbic acid

Ascorbic acid 4 g/day increases uric acid clearance in volunteers (23), although it does not reduce protein-bound uric acid in blood. Ascorbic acid 4-12 g/day causes acidification of the urine, which can cause precipitation of urate and cystine and consequently formation of urate stones or cystinuria. Ascorbic acid is excreted largely as oxalate, and hyperoxaluria results when large doses are... 

Whole blood ascorbic acid values may be a less sensitive indicator of vitamin C nutriture than serum or plasma levels of the vitamin because the vitamin C content in erythrocytes never falls to the low levels found in serum or plasma (89,90). Also there are no well-established classifications available relating blood vitamin C values to the nutritional status of this vitamin in a population (88). 

E.P., Gross, M., Cutler, R.G., Morris, J.S., Spate, V.L., and Helzlsouer, K.J., The risk of developing lung cancer associated with antioxidants in the blood ascorbic acid, carotenoids, alpha-tocopherol, selenium, and total peroxyl radical absorbing capacity. Cancer Epidemiol. Biomarkers Prev., 6, 907, 1997. 

Other instances in which the blood ascorbic acid has been reported to be altered by a variety of pathological circumstances, have been interpreted elsewhere (Selye, 1951) in terms of the G-A-S theory. 

Ascorbic acid uptake by these two cells is dependent on their metabolic activity and extracellular sodium concentration. In contrast, ascorbic acid uptake by the other lung cells does not exhibit saturation kinetics and is not dependent on metabolism or extracellular sodium (Castranova et al, 1983). This implies that uptake of ascorbic acid by other lung cells is a passive process and that the ascorbic acid content of these cells is dependent on the plasma level of ascorbic acid. Exposure of the lung to high concentrations of oxidants (for example, during smoking), which reduce blood ascorbic acid, will inevitably render these cells more susceptible to oxidant injury. 

Epidemiological studies have shown the elfect of smoking in reducing ascorbic acid levels in blood (Pelletier, 1970). Exposure to ozone and nitrogen dioxide also reduces blood ascorbic acid content. Unusually low amounts of ascorbate in milk of lactating women smokers have also been reported (Kallner et aL, 1981). This is attributed to the increased need for reducing agents imposed by chemical oxidants contained in tobacco smoke and some metabolic properties of nicotine (Bucca et al., 1989). This explains why the daily intake of ascorbic acid of at least 140 mg is required for smokers to reach a body pool of ascorbic acid comparable to that of nonsmokers, for whom a daily intake of about 100 mg is sufficient (Kallner et aL, 1981). 

However, this is true only for the sample solutions which contain a single component, H2O2 in this case. The electrochemical response is more complicated if sample solutions contain two or more redox species because both species would be oxidized or reduced, and thus they contribute concurrently to the output current. This is often the case for the electrochemical determination of drugs and metabolites or other biological components in blood because many kinds of redox-active species are intrinsically contaminated in blood. Ascorbic acid (vitamin C) and uric acid (UA) are redox species found in blood, and these compounds often disturb electrochemical measurements of blood because the redox potential... 

In 14 subjects 2-6 hours after ingestion of 4 g ascorbic acid the fractional clearance of uric acid increased to 202 41%. Ascorbic acid did not diminish protein-bound uric acid (31 -). A glycogenolytic effect of ascorbic acid was seen in rats after administration of 100 mg ascorbic acid. There was a significant decrease in liver glycogen, significant increase in liver ascorbic acid, blood ascorbic acid and increase in blood glucose (32 ). 

Of the water-soluble vitamins, intakes of nicotinic acid [59-67-6] on the order of 10 to 30 times the recommended daily allowance (RE)A) have been shown to cause flushing, headache, nausea, and moderate lowering of semm cholesterol with concurrent increases in semm glucose. Toxic levels of foHc acid [59-30-3] are ca 20 mg/d in infants, and probably approach 400 mg/d in adults. The body seems able to tolerate very large intakes of ascorbic acid [50-81-7] (vitamin C) without iH effect, but levels in excess of 9 g/d have been reported to cause increases in urinary oxaHc acid excretion. Urinary and blood uric acid also rise as a result of high intakes of ascorbic acid, and these factors may increase the tendency for formation of kidney or bladder stones. AH other water-soluble vitamins possess an even wider margin of safety and present no practical problem (82). 

Absorption, Transport, and Excretion. The vitamin is absorbed through the mouth, the stomach, and predominantly through the distal portion of the small intestine, and hence, penetrates into the bloodstream. Ascorbic acid is widely distributed to the cells of the body and is mainly present in the white blood cells (leukocytes). The ascorbic acid concentration in these cells is about 150 times its concentration in the plasma (150,151). Dehydroascorbic acid is the main form in the red blood cells (erythrocytes). White blood cells are involved in the destmction of bacteria. 

Up to 80% of oral doses of ascorbic acid are absorbed in humans with intakes of less than 0.2 g of vitamin C. Absorption of pharmacological doses ranging from 0.2 g to 12 g results in an inverse relationship, with less than 20% absorption at the higher doses. A single oral dose of 3 g has been reported to approach the absorptive capacity (tissue saturation) of the human intestine. Higher blood levels can be attained by providing multiple divided vitamin C doses per day. 

Ascorbic acid—vitamin C—is an essential nutrient that the human body cannot manufacture from other compounds. It is needed for the formation of collagen, the protein that makes up connective tissue, and is essential to muscles, bones, cartilage, and blood vessels. It is a strong antioxidant, preventing damage from oxygen free radicals. 

Garg A, Kunwar K, Das N, et al. 1980. Endosulfan intoxication Blood glucose, electrolytes, Ca levels, ascorbic acid and glutathione in rats. Toxicol Lett 5 119-123. 

Nowadays, consumers would like those antioxidants present in food products not only to stabilise food lipids, but also to be absorbed through the intestinal wall and protect the lipids of blood plasma against oxidation. This effect is relatively evident in the case of tocopherols (which are liposoluble) or ascorbic acid (which is hydrophilic), but much less evidence is available on antioxidants of medium polarity, such as flavonoids, rosemary oleoresins or green or black tea catechins. 

Choi, M.H., Kim, G.H., and Lee, H.S., Effects of ascorbic acid retention on juice color and pigment stability in blood orange Citrus sinensis) juice during refrigerated storage, Food Res. Int, 35, 753, 2002. 

Kinsey, V.E. (1947). Transfer of ascorbic acid and related compounds across the blood-aqueous barrier. Am. J. Ophthal. 30, 1262-1266. 

Pectin is found in apples and in the white membrane that surrounds the sections of oranges, grapefruits, or other citrus fruits, as well as in several other sources. Powdered pectin made from apple cores is also available, but scientists have found that eating apples or citrus fruit has a much better effect on lowering blood cholesterol levels than eating powered pectin does. They believe eating the whole fruit is better because the body also needs vitamin C to convert cholesterol into bile acids. Fruits contain vitamin C, or ascorbic acid, but the powdered pectin does not. 

A typical time course of PCL with luminol as the photosensitizer is shown in Figure 5, as blank. The presence of a water-soluble antioxidant leads to dose-dependent temporary inhibition of PCL. ACW (antioxidant capacity of water-soluble compounds) represents the effect of human blood plasma (2 p.L) on PCL all tested antioxidants, such as ascorbic acid, uric acid, Trolox, taurine, bilirubin, ceruloplasmin, etc., produced the same effects. 

Basic procedure (ACW kit) Mix 1500 pL of ACW reagent 1 (diluter) with 1000 pL of ACW reagent 2 (buffer) and 25 pL of photosensitizer reagent (lumi-nol based). Start measurement after brief vortexing. Assayed solution (or control) is added before addition of photosensitizer reagent. Volume of ACW reagent 1 is reduced by the volume of assayed plasma sample. Standard substance ascorbic acid. Duration of measurement 2-3 min. Measured parameter effective lag phase = lag-phase sample - lag-phase blank. Assayed amount of human blood plasma 2 pL. 

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. 

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