Ascorbic acid history

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Deficiency of ascorbic acid leads to scurm/, which is characterised by petechial haemorrhages, haematomas, bleeding gums (if teeth are present) and anaemia. It has a memorable place in the history of therapeutic measurement. 

I. Plasma Ascorbic Acid Levels. The measurement of plasma levels of ascorbic acid in populations has been used to provide more reliable data on average intakes than that obtained from the incidences of scurvy or from nutritional histories. It must be emphasized, however, that scurvy develops only in those individuals with plasma levels below those which can be accurately measured. Extensive studies have provided empirical correlations of expected plasma and white blood cell levels with different ascorbic acid intakes (L24, M24, S23). Other studies have also shown that both the ascorbic acid and the dehydroascorbic acid content of foods were equally effective in raising the plasma level of ascorbic acid (D8). 

At the conclusion of the Medical Research Council study, saturation tests were done on the subjects with long histories of accurately known ascorbic acid intakes. More than three daily test doses (10 mg/kg body weight) were necessary before a sharp rise occurred in urinary ascorbic acid excretion of subjects who had been receiving 20 mg/day or less, but again no distinction could be made in this way between the deficient and the protected individuals receiving the lower amounts. 

Photocatalytic Polymers. The electrochemical experiments cited above were chosen from a vast body of recent polymer coated electrode work. Likewise the field of polymer supported photoredox catalysts is also broad and has a more extended history. Possibly a common linkage between electrochemical and photochemical catalyses, assisted by polymers, can be traced to oxidation of ascorbic acid (AH2). In 1966 Davidov (20a) found that light exposed, polyacrylonitrile (PAN) containing solutions of AH2 consumed oxygen in a measurably different manner than similar solutions without AH2. (Simple photoabsorption of 02 also occurs). 

One feature of ascorbic acid that attracted attention early in its history was that it appeared to be present in the body largely in the reduced state (AA), despite the fact that it is readily oxidized to dehydroascorbic acid (DHA) in vitro. Indeed it became, for a time, a convenient but unjustified assumption that the vitamin existed wholly in the reduced form in body tissues and fluids, and therefore could be estimated quite simply by methods employing the reduction of 2 6-dichlorphenolindo-phenol. Today it is clear that if the whole vitamin content is to be accurately measured, it is necessary to estimate both AA and DHA, e.g., by the method of Roe and Kuenther (1943). 

The history of vitamin C is common knowledge. In the mid-18th century James Lind demonstrated that the juice of fresh citrus fruits cures scurvy (197). The active agent, the enolic form of 3-keto-L-gulofuranlactone, christened ascorbic acid or vitamin C, was isolated in the late 1920 s by Albert Szent-Gybrgyi (317). By the mid-1930 s, methods had been devised to synthesize the compound, and it soon became widely available at low cost. It was soon established that the substance was virtually nontoxic at any dosage. The structure of vitamin C is shown in Chart 1. 

The memorial plaque is not the only tribute to the early history of biocatalysis at Birmingham. The Frankland Building commemorates Percy Frankland, who was professor of chemistry at Mason College, and whose views of biocatalysis have already been noted (Frankland, 1897). The Howarth Building commemorates the leader of the group at Birmingham responsible for their synthesis of L-ascorbic acid (Scheme 1.9). 

The storage of plasma or serum samples for periods of several years is now common in connection with health surveys of various kinds. Whether or not the values obtained for retinoids as well as for other labile substances such as vitamin E and ascorbic acid are still valid after extensive storage is of critical concern. Methodological problems did arise in two studies (Kark et al., 1981 Wald et al., 1980) in which plasma samples stored for long periods were analyzed for retinol relative to cancer risk. In Kark s study (1981) the history of the samples was not well documented, including the number of times that specific samples were frozen and thawed, and in Wald s study (1980) about one-fourth of the samples, including 40% of the samples from cancer subjects, arrived at the analytical laboratory in cracked tubes. 

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