Guinea pigs, ascorbic acid requirement

Estimates of ascorbic acid requirements can be small, for the amount to maintain histologically normal teeth in the guinea pig, or large, for the amount necessary to maintain blood levels equal to those of animals who synthesize their own ascorbic acid. The limits of the minimal protective dose against scurvy and the saturating dose are well known in guinea... 

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). 

C14. Collins, M., and Elvehjem, C. A., Ascorbic acid requirement of the guinea pig using growth and tissue ascorbic acid concentrations as criteria. /. Nutrition 64, 503-511 (1958). 

P8. Pfander, W. H., The effects of iodinated casein, thiouracil and cortisone on the ascorbic acid requirement of the male guinea pig. /. Nutrition 47, 487-501 (1952). 

There is, without doubt, a wide spread between the amount of vitamin C needed to prevent frank scurvy and that required for the maintenance of best health. In young growing guinea pigs about 0.5 mg. ascorbic acid per day will protect against scurvy symptoms, but there are distinct gains in health when the intakes are up to 10 times this amount.46... 

Vitamin C is L-ascorbic acid (chemically 2-oxogulonolactone). The two hydroxyl groups have acidic properties. By releasing a proton, ascorbic acid therefore turns into its anion, ascorbate. Humans, apes, and guinea pigs require vitamin C because they lack the enzyme L-gulonolactone oxidase (tl.3.8), which catalyzes the final step in the conversion of glucose into ascorbate. 

Until the 20th century, it was thought that scurvy was confined to humans. Most plants and animals have the ability to synthesize ascorbic acid, but it was discovered that a limited number of animals, including primates, guinea pigs, the Indian fruit bat, and trout, also lack the ability to produce ascorbic acid. In vertebrates, ascorbic acid is made in the fiver from glucose in a four-step process. Each step requires a specific enzyme and humans lack the enzyme required for the last step, gulonolactone oxidase. 

Ascorbic acid (vitamin C) is a water-soluble vitamin but is not part of the B group. It is a metabolic requirement for all species but is a dietary requirement only for those that lack the enzyme for its synthesis (primates, guinea pigs, certain birds, fish). Therefore, it is not required in poultry diets. It is involved in the formation and maintenance of intercellular tissues having collagen or related substances as basal constituents. 

The ability to synthesise ascorbic acid from glucose is absent in a small group of animal species that include man, primates, the guinea pig and the fruit-bat this is due to the absence of the gene that codes for one of the enzymes required for ascorbate synthesis. These species are therefore dependent on an external source of the vitamin in their diet and it is needed as a cofactor for several hydroxylase enzymes, notably the iron-dependent proline and lysine hydroxylases and the copper-dependent dopamine-(3-hydroxylase the function of ascorbate in these enzymes is likely to be its ability to keep the metal in the reduced form which is necessary for hydroxylation. The ability of ascorbate to reduce Fe3+ to Fe2+ is important in promoting the gastrointestinal uptake of iron and for its release from the iron store ferritin. 

Scorbutic guinea pigs develop hypercholesterolemia, which may lead to the development of cholesterol-rich gallstones. This is largely the result of impaired activity of cholesterol 7-hydroxylase, which is an ascorbate-dependent enzyme (Section 13.3.8), resulting in reduced oxidation of cholesterol to bUe acids. There is no evidence that increased intakes of vitamin C above requirements result in increased cholesterol catabolism. 

Experimental alkaptonuria has also been produced in rats on a diet de-ficent in sulfur-containing amino acids (295). Similar excretory patterns were produced after additional phenylalanine, tyrosine, or their corresponding keto acids, and the condition was relieved on gi dng cysteine, but not ascorbic acid (644). Moreover the p-hydroxyphenylpyruvate excretion was much lower, relative to the homogentisic acid excretion, than in the type of ascorbate-dependent alkaptonuria studied by Sealock in the guinea pig (rats cannot in any case be made ascorbic acid-deficient). Xeuberger and Webster (644) also showed that this second type of experimental alkaptonuria could be produced in many types of amino acid imbalance, or in protein deficiency, and that the threshold intake of phenylalanine or tyrosine required to produce the condition varied with the nutritional state and also with the acid-base balance, acid urines being associated with a decreased homogentisic acid excretion (cf. also 150, 273, 787). 

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