Abstract
IT is well known that dietary deficiencies can be seriously aggravated by the induction of a hyperthyroid state. Recently it has been shown1–3 that selenium significantly prolongs the survival-time of rats and prevents the onset of the liver necrosis which follows the ingestion of a diet containing yeast as the only source of protein. This protective effect of selenium resembles that shown by a number of apparently unrelated substances such as methionine, cystin, vitamin E, methylene blue and methylthiouracil, the mode of action of which is not understood. Unpublished observations, made in the course of a systematic investigation into the effects of various hormonal and nutritional stimuli on the course of liver necrosis, had suggested that it might be possible to distinguish between a true protective effect and a ‘non-specific’, indirect effect of the substances tested by the induction of a hyperthyroid state. Methyl -thiouracil, for example, which protects the euthyroid weanling rat against the onset of liver necrosis, was ineffective in litter-mates made hyperthyroid by the simultaneous addition of thyroid powder to the diet. A somewhat similar effect was seen if methylene blue was given, in contrast to the persistence of the protective effect obtained if vitamin E was used. In the light of these considerations it was thought of interest to see how the induction of a hyperthyroid state would affect the protective effect of selenium in dietary liver necrosis.
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References
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ATERMAN, K. Selenium and Liver Necrosis in the Hyperthyroid Rat. Nature 182, 1514 (1958). https://doi.org/10.1038/1821514a0
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DOI: https://doi.org/10.1038/1821514a0
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