Scurvy in guinea pigs

Partial protection from scurvy in guinea pigs provided by a-lipoic acid (R22) is probably due to the preservations of small residual amounts of ascorbic acid in the diet. Ascorbic acid has similar effects on riboflavin-(T4) and thiamine-deficient (T3) rats. The temporary improvements are the result of the reduction of thiamine disulfide to nutritionally active forms (B3). 

Scurvy in guinea pigs, uncomphcated by other known dietary deficiencies, has been possible only in recent years (R6). The earlier experi-... 

Anemia has frequently, but not consistently, been reported in association with scurvy in clinical cases, both in adults and infants, and in experimental scurvy in guinea pigs and monkeys. The extensive literature has been cited (M18, L19, V2). The anemias were not constant in type or severity, although all were reheved when ascorbic acid was reintroduced to tbe diet. In contrast, no anemia or abnormality of the blood picture was ever seen in experimental human scurvy. The therapeutic effect of ascorbic acid on the anemia cannot be accepted as proof of its etiology, since associated deficiencies would also be made good with the return of normal appetite. It is well recognized that the clinical cases of scurvy usually have associated deficiencies. Often, there is iron deficiency in the milk-fed infants, and folic acid or vitamin B12 deficiency in the malnourished adult. ... 

The half-life of ascorbic acid is inversely related to the daily intake and is 13—40 d in humans and 3 d in guinea pigs, which is consistent with the longer time for humans to develop scurvy. 

With respect to human beings there is some question as to what level of tissue saturation should ideally be maintained. In guinea pigs defects in developing incisors appear when the tissue concentrations are about 40 per cent of the maximum. Scurvy symptoms do not appear until the tissue saturation has reached a much lower level (about 20 per cent saturation). It seems logical to suppose that in different individuals the manifestations of mild vitamin C deficiency would be different and that a high degree of saturation would be safest from the standpoint of all the vulnerable tissues. 19... 

Holst and Frolich, in 1907. first deirxinstrated that scurvy could be produced in guinea pigs. A comparable condition cannot be produced in rats. 

The development of scurvy in the guinea pigs is much more rapid than in man, as would be expected from the higher requirement per unit body weight and the shorter half-life of ascorbic acid in guinea pigs. 

Changes in the serum and plasma protein fractions in vitamin C deficiency in guinea pig have been reported in addition to the increased fibrinogen already mentioned. Howard (H18) did not find any difference in the total plasma protein ccmcentrations or in the electrophoretic mobility on paper of plasma proteins from normal and scorbutic guinea pigs. However, in both acute and chronic scurvy, the amount of plasma albu-... 

Cortisone or ACTH administration did not alter the ascorbic acid requirements of guinea pigs for prevention of scurvy (P8, H7). As would be expected, ACTH or cortisone did not diminish the antiscorbutic effectiveness of dehydroascorbic acid in guinea pigs (C13), nor did they affect the plasma levels in patients with rheumatoid arthritis (Ml). Both ACTH and cortisone do, however, increase the excretion of ascorbic acid in the urine on large intakes (Kl). 

Nadel and Schneider (1951) have reported a fivefold increase in the excretion of formaldehydogenic substances in guinea pigs suffering from advanced scurvy. 

Chojkier, M., Spanheimer, R., and Peterkofsky, B., 1984, Specifically decreased collagen biosynthesis in scurvy dissociated from an effect on proline hydroxylation and correlated with body weight loss In vitro studies in guinea pig calvarial bones, J. Clin. Invest. 72 826-835. 

In 1907, Holst and Frolich, of Norway, produced scurvy experimentally in guinea pigs by feeding them a diet deficient in foods containing ascorbic acid. 

In 1932, Charles Glen King and W. A. Waugh, at the University of Pittsburgh, isolated from lemon juice a crystalline material that possessed antiscorbutic activity in guinea pigs this marked the discovery of vitamin C, a deficiency of vv ich caused the centuries-old scourge of scurvy. 

Research lea ding to the discovery of vitamin C began in 1907 when it was observed by Axel Holst and Theodor Ern hlich that guinea pigs were as susceptible to scurvy as humans and that the disease could be produced experimentally in these animals (8). These findings led to the development of an assay for the biological deterrnination of antiscorbutic activity of food products (9). 

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