Scurvy ascorbic acid concentration

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). 

C is rapidly excreted. About 4% of this pool is lost daily (fractional catabolic rate) after intermission of vitamin C supply. The biological half-time of the pool is therefore approximately 8-40 days (Homig, 1981). The first symptoms of scurvy occur upon reaching a total body pool of 300-400 mg. Table II shows data on the turnover rate of ascorbic acid for man and different species. Table III shows the ascorbic acid concentrations in organs and body fluids of the adult man. 

As mentioned above, ascorbic acid acts as a neuroprotective agent in in vitro models of scurvy. Therefore, it is a surprise that no symptoms of brain cell damage have been reported in conditions involving severe systemic ascorbic acid deficiency. This may be explained by the fact that the scorbutic state cannot be produced in the intact animal brain because of the brain s homeostatic mechanisms such as the highly specific ascorbic acid transport system in the choroid plexus (Spector, 1989) and the inability of ascorbic acid to cross the blood-brain barrier, which effectively isolate the ascorbic acid content of the intact brain from the rest of the body s ascorbic acid pool. The active transport of ascorbic acid from blood to cerebrospinal fluid (Spector and Eells, 1984), together with cellular uptake mechanisms, represents the base for homeostasis of brain ascorbic acid concentrations (see also Section 2). This is in agreement with the report about normal ascorbic acid concentrations in brains from patients with Parkinson s disease (Riederer et al., 1989), in which free radical damages are postulated to be involved (see below). 

In 1795 the British admiralty finally mandated a ration of concentrated lime or lemon juice for all British sailors (hence the name limeys ). Scurvy continued to be a problem in some other parts of the world until 1932, when Hungarian scientist Albert Szent-Gyorgyi, and W. A. Waugh and C. G. King at the University of Pittsburgh, isolated and synthesized ascorbic acid. 

Ascorbic Acid Deficiency. Scurvy is the classical disease associated with ascorbate deficiency. It is a disease of the connective tissue and probably is caused by inadequate crosslinking attributed to a lack of hydroxy-lated proline and lysine. Many consider scurvy to be an advanced stage of ascorbate deficiency. Chronic deficiencies may also (l)in-crease risk for malignancies, as evidenced by oxidized DNA markers and increased concentrations of reactive oxygen species (2) decreased immune function, as evidenced by less vitamin in neutrophils and lymphocytes (3) cardiovascular disease caused by the inflammatory response on the blood vessel walls and (4) cataract formation caused by decreased concentrations of ascorbate in the ocular tissues. 

Tests measuring the plasma ascorbic acid levels a few hours following the test dose were more useful for rapid evaluation of tissue storage of ascorbic acid (W7, S26, RIO). The clinical usefulness of such a test was reported (D23) in a trial in which nine scorbutic patients had serum concentrations less than 0.25mg/100ml three hours after an oral dose of 15 mg ascorbic acid/kg body weight. Some individuals with normal intakes and low initial levels also had equally small rises. But rises to levels greater than 0.25 mg/100 ml were not consistent with scurvy. 

Some coenzyme measurements have been reported which should be related to the changes in enzyme activities. Scurvy decreased liver cocarboxylase concentration by half (B20) but did not alter pyridine nucleotide coenzymes (Bll). Rats fed extra ascorbic acid (100 mg/day) had a decreased liver coenzyme A content of about 40 % after three days (C2). 

Related to, but distinct from, metabolic substitution or replacement is metabolic enhancement where it is visualized that flavonoids could act syner-gistically with ascorbic acid. This would increase the biological potency of the acid but would not necessarily result in elevated concentrations of it in tissues. In areas where ascorbic acid has supposed metabolic involvement distinct from the simple prevention of scurvy, there is little evidence that flavonoids enhance or potentiate the ascorbic acid activity [80,81]. In a recent study of the influence of the acid on the incidence of the common cold in a group of 350 young persons, a daily dose of 80 mg synthetic ascorbic acid significantly depressed by 18% the number of symptoms recorded this too was the extent of the reduction in a parallel group on 80 mg of the acid as orange juice [59]. It would never ... 

Mental symptoms (depression) accompany the physical symptoms of vitamin-C deficiency disease (scurvy). In 1957, Akerfeldt reported that the serum of schizophrenics had been found to have greater power of oxidizing N,N-dimethyl-p-phenylenediamine than that of other persons. Several investigators then reported that this difference is due to a smaller concentration of ascorbic acid in the serum of schizophrenics than of other persons. This difference has been attributed to the poor diet and increased tendency to chronic infectious disease of the patients (Benjamin, 1958 Kety, 1959), and has also been interpreted as showing an increased rate of metabolism of ascorbic acid by the patients (Hoffer and Osmond, 1960 Briggs, 1962). It is my opinion, from the study of the literature, that many schizophrenics have an increased metabolism of ascorbic acid, presumably genetic in origin, and that the... 

Ascorbate and Hormone Balance. The highest concentrations of ascorbate are found in the adrenal and pituitary glands, and the terminal stages of scurvy are just preceded by complete depletion of adrenal ascorbate, leading, it has been frequently stated, to scurvy death from adrenocortical failure. This has caused many to suggest that the ascorbic acid-dehydroascorbic acid system plays an important role in the synthesis and release of hormones of the adrenopituitary axis. The evidence for this is both conflicting and confusing (13, 72, 73,102, 277, 278). 

The minimum vitamin C requirement to prevent the development of scurvy has been found to be 10 mg/day (Hodges et al., 1971). This supply is not sufficient for the provision of acceptable reserves of the vitamin. The intake of 10 mg ascorbic acid per day reflects a plasma concentration of 7.6-14.1 p,mol/liter (0.13-0.24 mg/100 ml), a concentration that is far from tissue saturation. The renal clearance of ascorbic acid rises sharply at a point of 82 xmol/liter (1.4 mg/100 ml). An adequate plasma level of 44 p.mol/liter (0.75 mg/100 ml) can be maintained by a daily supply of 60-75 mg ascorbic acid. The daily amount of ascorbic acid, which is catabolized by the human body, can be calculated to be 60 mg based on a total body pool of ascorbic acid of approximately 1500 mg and a maximum turnover rate of 4%. These data are the scientific basis for the formulation of the above recommendations to meet the physiological needs. Table IV shows the recommended daily vitamin C intake for different population groups from the different societies that issue such recommendations. 

The concentration of ascorbic acid in the white cell-platelet layer of blood is a much better index of tissue concentration and body stores of vitamin C then the level in plasma. In normal subjects whose tissues are nearly saturated, the white cell-platelet concentration is 25 to 30 mg. per 100 ml. The concentration falls gradually during depletion and reaches zero shortly before signs of scurvy make their appearance. Peters and associates228c suggest that a white cell-platelet concentration of less than 2 mg. per 100 g., on repeated analyses, supports the diagnosis of scurvy. 

Absorption of vitamin C from the small intestine is a carrier-mediated process that requires sodium at the luminal surface. Transport is most rapid in the ileum and resembles the sodium-dependent transport of sugars and amino acids, but the carrier is distinct for each class of compound. Some ascorbate may also enter by simple diffusion. With dietary intake less than 100 mg/d, efficiency of absorption is 80-90%. With intake equal to the RDA, plasma ascorbate is 0.7-1.2 mg/dL, and the ascorbate pool size is 1500 mg. Scurvy becomes evident when the pool is less than 300 mg, at which point plasma ascorbate is 0.13-0.24 mg/dL. Highest tissue concentrations of ascorbate are in the adrenal gland (cortex > medulla). 

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