Ascorbic acid catabolism in guinea pigs.

نویسنده

  • L L SALOMON
چکیده

There have been numerous reports suggesting that the metabolism of ascorbic acid in humans and in animals is affected by stress.l However, detailed information which would permit an analysis of the underlying mechanism is not available. From the variety of effects cited, it would appear that no single mechanism can explain all of the findings. It has been suggested that increased ascorbic acid requirements exist in stress either because of increased utilization (2) or because of increased catabolism (1). These two factors are not synonymous, since utilization implies the retention of the intact ascorbic acid molecule or dehydroascorbic acid, and catabolism infers the destruction of the molecule beyond the dehydroascorbic acid stage. A choice between these mechanisms is, moreover, difficult or impossible to make under ordinary circumstances because the products of complete catabolism of ascorbic acid cannot be specifically determined, except with tracer techniques (4, 5). The availability of ascorbic acid-l-C4 made it possible to resolve some of these difficulties and investigate certain aspects of this important problem in more detail. The present communication deals specifically with the fate of ascorbic acid after equilibration with body ascorbic acid, in contradistinction to the metabolism of newly administered ascorbic acid in the intact guinea pig. In one series of experiments, the rate of ascorbic acid loss by the diphtheria-intoxicated guinea pig was investigated. The effects of the toxin in guinea pigs are consistent and reproducible. Among the consequences produced by its administration is a decrease in ascorbic acid in several tissues (6), characteristically pronounced in the adrenal glands. Scorbutic guinea pigs also show lowered resistance to the toxin (7). Preliminary work had shown that urinary excretion of ascorbic acid radioactivity did not differ significantly between toxin-treated and control guinea pigs, although there was some reason to believe that respiratory

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عنوان ژورنال:
  • The Journal of biological chemistry

دوره 228 1  شماره 

صفحات  -

تاریخ انتشار 1957