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Companion Animals: Vitamin C

Deficiency

Clinical signs of scurvy or vitamin C deficiency in those species that cannot synthesize the vitamin include weakness, fatigue, bone pain, loose teeth and hemorrhages of the skin, musculature, adipose tissue and certain organs. Dogs and cats, however, have the capability to synthesize vitamin C and, therefore, would not be expected to show these deficiency signs under normal conditions. However, some studies with dogs have shown that the ability to synthesize vitamin C is compromised under conditions of stress or disease. Starvation or lack of optimum food supplies will affect vitamin C synthesis. Mean plasma ascorbic acid concentration was significantly lower in dogs after they were fasted (Lee et al., 1986). Also, some of the benefits of supplemental vitamin C are with pharmacological doses of ascorbic acid (e.g., 3,000 mg intravenously per day), which may be quite distinct from its nutritional contribution.

Completely satisfactory and reliable procedures to assess vitamin C nutritional status have not been developed because of limited knowledge concerning the vitamin's metabolic functions. However, information concerning adequacy has been determined by an analysis of vitamin C concentrations in serum (plasma), leukocytes, whole blood, or urine. Normal serum ascorbic acid values in dogs should exceed 1.0 mg per 100 ml (Ralston Purina, 1987). Leukocyte vitamin C concentrations provide information concerning body stores of ascorbic acid (Turnbull et al., 1981). Precautions need to be taken to protect the vitamin in solution and to select an assay that measures the vitamin itself and not other substances present.

A. Deficiency in Dogs

Scurvy in dogs has been reported (Garlick, 1946; Meier et al., 1957; Holmes, 1962; Hunt, 1962; Vaananen and Wikman, 1979; Kolb, 1984). There is controversy about the therapeutic use of ascorbic acid in canine diseases.

Vitamin C deficiency also has been reported to be associated with canine hypertrophic osteodystrophy (HOD) (Grondalen, 1976). This disease affects young, rapidly growing dogs. It is characterized by an enlarged metaphysis of long bones. Hemorrhages are common in the region of bone disorganization. The clinical findings of the acute stage are hyperthermia, anorexia and inability to stand because of great pain in the extremities (Grondalen, 1976). Meier et al. (1957) found that dogs with HOD had low plasma ascorbic acid concentrations and large doses of vitamin C (100 mg to 200 mg) given orally or IM enhanced healing. Supplementation with ascorbic acid is not always effective. Teare et al. (1980) reported that 600 mg of ascorbic acid twice daily only aggravated the skeletal disease induced by overfeeding protein, energy and calcium to Labrador retriever puppies. The study was weakened by the fact that the pups evaluated did not have clinical signs of acute HOD, which include both lameness and low blood ascorbic acid.

B. Deficiency in Cats

Controlled studies evaluating the need for supplementation or describing specific deficiency of vitamin C in cats have not been published. A number of trials have failed to demonstrate a need for dietary ascorbic acid in cats (Carvalho da Silva, 1950). Successful growth and reproduction are routinely obtained with commercial and purified (NRC, 1986) diets containing no supplemental ascorbic acid.

As in dogs, vitamin C synthesis in cats is lower than in other species, including the cow, sheep, rat and rabbit (Rucker et al., 1980). Pietronigro et al. (1983) reports that central nervous system function following spinal cord injury in the cat was associated with large doses of ascorbic acid from the region of the injury. Treatment of injury with two drugs (naloxone or methyl-prednisolone) preserved neurological function and prevented vitamin C loss.

 

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