Ascorbic acid vitamin excretion

Uronic acids are biosynthetic intermediates m various metabolic processes ascorbic acid (vitamin C) for example is biosynthesized by way of glucuronic acid Many metabolic waste products are excreted m the urine as their glucuronate salts... 

Ascorbic acid is very soluble in water and mainly excreted in the urine. No ascorbic acid is excreted during vitamin C deficiency. A minimum amount is lost in the feces, even after intake of gram dosages (154). 

To enhance iron excretion, intensive chelation therapy is used. The most successful drug is desferrioxamine B, a powerful Fe3+-chelator produced by the microbe Streptomyces pilosus,6 The formation constant for the Fe(III) complex, called ferrioxamine B, is 103afi. Used in conjunction with ascorbic acid—vitamin C, a reducing agent that reduces Fe3+ to the more soluble Fe2+— desferrioxamine clears several grams of iron per year from an overloaded patient. The ferrioxamine complex is excreted in the urine. 

If the drug taken in overdose is a base, for example, a benzodiazepine tranquilliser or an antihistamine, excretion should be favoured by acidification of the urine. Agents that may be used to achieve this include ammonium chloride, NH Cl- (an acidic salt by partial hydrolysis) and ascorbic acid (vitamin C). If the pH of the urine is artificially lowered, the technique is called forced acid diuresis. 

Glyoxalate can be transaminated to glycine, reduced to glycolate, converted to a-hydroxy-/3-ketoadipate by reaction with a-ketoglutarate, or oxidized to oxalate and excreted in urine. The first three reactions require pyridoxal phosphate, NADH, and thiamine pyrophosphate, respectively. In humans, ascorbic acid (vitamin C) is a precursor of urinary oxalate (Chapter 38). Since calcium oxalate is poorly soluble in water, it can cause nephrolithiasis and nephrocalcinosis due to hyperoxaluria. 

Administration of vitamin A has been proposed for the treatment of cases of the Hunter and Hurler syndromes, but this therapy seems to be detrimental (Ml), the urinary glycosaminoglycan excretion rate being increased in a case of the Hurler syndrome (D3). L-Ascorbic acid (vitamin C) increases the level of dermatan sulfate in cultured Hurler fibroblasts (S6, S7), but not in the normal cells. Furthermore, L-ascorbic acid causes selective retention of sulfate-containing glycosaminoglycans vwthin the abnormal cell (S7). However, it is possible that dietary therapy could be of some assistance. 

A study in 13 healthy subjects given aluminium hydroxide 900 mg three times daily found that ascorbic acid (vitamin C) 2 g daily increased the urinary excretion of aluminium threefold. Ascorbic acid significantly increases the concentration of aluminium in the liver, brain, and bones of rats given aluminium hydroxide. ... 

The most convincing evidence that ascorbic acid can be synthesized from a hexose sugar in animals comes from the work of Jackel and his collaborators (1950). When D-glucose labeled uniformly in all positions with was supplied to rats which had been fed chloretone to stimulate the synthesis of the vitamin, L-ascorbic acid was excreted which was also labeled uniformly. This clearly indicates that n-glucose can serve as an ultimate precursor but does not exclude the possibility that the glucose may have to be converted to other sugars before being transformed. 

Hyperoxaluria can be induced by vitamin C. Investigations in healthy women have shown that less than 20% of ingested doses of ascorbic acid are excreted in the urine in the first day while by the second day after supplementation both plasma and urine levels are indistinguishable from those of the controls. In some healthy women ascorbate excretion did not rise even with 6 g. A dose of 8 g ascorbic acid, however, resulted in a rise of excretion from 30 mg to 250 mg/24 hours. The results suggest that in healthy women the vitamin C is excreted as oxalate or dehydroascorbic acid (28 ). 

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. 

Biosyntheses of hexuronic acids and L-ascorbic acid in plants and animals are closely related. Hexuronic acids, L-ascorbic acid, and L-tartaric acid (a possible precursor of dihydroxyfumaric acid) commonly occur together in plants. If a rat is given chloretone (an antispasmodic), both L-ascorbic acid and D-glucuronic acid are excreted in increased quantity.244 Unlike humans, rats can synthesize their own vitamin C, and are therefore independent of outside sources. Here, D-glucose and D-galactose can be utilized, but not D-mannose. 

Chromium compounds interact synergistically or antagonistically with many chemicals. For example, potassium dichromate administered by subcutaneous injection potentiated the effects of mercuric chloride, citrinin, and hexachloro-1,3-butadiene on rat kidneys (USPHS 1993). Chromium effects were lessened by ascorbic acid and Vitamin E, and N-acetyl cysteine was effective in increasing urinary excretion of chromium in rats (USPHS 1993)... 

Oral absorption of ascorbic acid is via an energy-dependent process that is saturable and dose-dependent. Ascorbic acid is stored in the body. Excessive amounts of consumed vitamin C, i.e. if daily intake surpasses 100 mg, are rapidly excreted in the urine. 

Mega vitamin intake of vitamin C may result in diarrhea due to intestinal irritation. Since ascorbic acid is partially metabolized and excreted as oxalate, renal oxalate stones may form in some patients. 

Oral contraceptives decrease the plasma levels of ascorbic acid. Aspirin also decreases tissue levels of vitamin C. The renal excretion of acidic and basic drugs may be altered when they are coadministered with large doses of vitamin C. 

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. 

ANTACIDS CONTAINING ALUMINIUM VITAMIN C t aluminium levels, with risk of encephalopathy in patients with renal failure Uncertain possibly t absorption due to ascorbic acid in the presence of 1 renal excretion Avoid co-ingestion in patients with renal failure... 

Disposition in the Body. Readily absorbed after oral administration the proportion of a dose absorbed tends to decrease with increasing dose it is widely distributed in the body tissues. The concentration of ascorbic acid is higher in leucocytes and platelets than in erythrocytes and plasma. Ascorbic acid is metabolised to dehydroascorbic acid, 2,3-diketogulonic acid, oxalate, and carbon dioxide some conjugation with sulphate occurs to form ascorbate-3-sulphate. Ascorbic acid in excess of the body s requirements is rapidly eliminated in the urine. About 85% of an intravenous dose, given to subjects previously saturated with the vitamin, is excreted in the urine in 24 hours, with about 70% of the dose excreted unchanged and 15% as dehydroascorbic acid and diketogulonic acid. The amount normally present in the body is in excess of 1.5 g. 

Vitamin C, or ascorbic acid, is important in the formation of collagen, a protein that holds together the connective tissues of skin, muscle, and blood vessels. Vitamin C is obtained from eating citrus fruits. A deficiency of vitamin C causes scurvy, a common disease of sailors in the 1600s who had no access to fresh fruits on long voyages. In Chapter 3, we learn why some vitamins like vitamin A can be stored in the fat cells in the body, whereas others like vitamin C are excreted in urine. 

Prieme, H Loft, S., Nyyssonen, K Salonen, J. T., and Poulsen, H. F. (1997). Mo effect of supplemental Inn with vitamin E, ascorbic acid, or coenzyme QIO on oxidative DNA damaj>e estimated by 8-oxy-7,8-dihydTQ-2-deoxyguanosinc excretion in smokers. Am. I. Clin. iVittr, 65, 503- 507,... 

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