Sulphonamides and Potato Starch Refection in the Rat

Coates, Michael I.; Henry, K. M.; Kon, P. M.; Kon, S. K.; Mawson, Elinor Huntsman; Stanier, J. E.; Thompson, S. Y.

doi:10.1038/157262a0

Cited by 11 publications

(2 citation statements)

References 9 publications

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“…tolerated antibiotics throughout the study. The time of onset or severity of signs of riboflavin deficiency did not appear to be influenced by antibiotic administration, although intestinal synthesis of riboflavin has been demonstrated in rats (67)(68)(69). Slight decreases in serum cholesterol have been noted in riboflavindeficient rats (70), but those observed in our patients more likely were related to the ingestion of safflower oil (71), since riboflavin therapy did not increase the serum cholesterol.…”

Section: Discussionmentioning

confidence: 39%

The Rapid Induction of Human Riboflavin Deficiency with Galactoflavin *

Lane¹,

Alfrey²,

Mengel³

et al. 1964

J. Clin. Invest.

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Signs of riboflavin deficiency require many months to develop in patients placed on riboflavinrestricted diets (1-6). The demonstrations that riboflavin deficiency induced by dietary restriction or riboflavin antagonists resulted in regression of rodent tumors (7-13) prompted several efforts in this laboratory to produce riboflavin deficiency in patients with neoplastic disease (14, 15). Riboflavin antagonists were used in these studies with the objective of producing the deficiency state rapidly, since a regimen requiring many months of dietary restriction would not lend itself to therapeutic evaluation in patients with metastatic cancer. These earlier investigations did not result in the production of clinical evidences of riboflavin deficiency or in objective demonstrations of tumor regression. The administered riboflavin antagonists, selected on the basis of their effectiveness in rats, were shown to be metabolized differently in man. The most active of these agents against rat tumors, 6,7-dimethyl-9-(2'-acetoxyethyl) -isoalloxazine, was rapidly and almost completely hydrolyzed in man, although a significant amount of the absorbed drug was excreted unchanged by rats. With the objective of producing human riboflavin deficiency, an analog was sought that would be an effective riboflavin antagonist in rodents and would be metabolized similarly in rodents and in man.The present paper describes studies with 1O-Ddulcityl -7,8-dimethyl-isoalloxazine, galactoflavin,

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Section: Discussionmentioning

confidence: 39%

The Rapid Induction of Human Riboflavin Deficiency with Galactoflavin *

Lane¹,

Alfrey²,

Mengel³

et al. 1964

J. Clin. Invest.

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“…We have known for some time that faeces of 'refected' rats or, as we should say more acurately now, of rats with undigested starch in their gut offering a richer pabulum to the microbial population, are richer in vitamins of the B complex than those of rats given an easily digestible carbo hydrate (Kon et al 1938). The capriciousness with which potato starch appears (Coates, Henry, Kon, Kon, Mawson, Stanier & Thompson 1946;Ford, Henry, Kon, Porter, Thompson & Wilby 1953) testifies differences in coprophagous inclinations of rats in various situations. Whether with 'refective' diets they manage to grow or not probably depends on the amount of faeces they choose to May I express my warm appreciation of the honour bestowed upon me on this occasion.…”

Section: Vitamins a And B1zmentioning

confidence: 99%

Vitamins A and B ₁₂ and some comments on refection

1962

Proc. R. Soc. Lond. B.

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I worked in Hopkins’s laboratory some 35 years ago, so I am deeply grateful for the opportunity to take part in this Symposium. It was suggested that I should deal generally with the biochemical side of vitamins, but in the time at my command I have chosen to deal with some facets with which I am acquainted. For my first theme I have singled out a few of the newer findings about vitamin A, which substance has interested us at Shinfield for quite a long time. Some 14 years ago Deuel and his collaborators in California (Mattson, Mehl & Deuel 1947; Wiese, Mehl & Deuel 1947), Morton and his collaborators in Liverpool (Glover, Goodwin & Morton 1947) and ourselves at Shinfield (Thompson, Ganguly & Kon 1947), showed that the conversion of carotene into vitamin A takes place in the small intestine. Shortly afterwards we learned that a German worker (Wagner 1939) had, well before that date, described the conversion of carotene into vitamin A in the intestine of the whale. We were intrigued by this finding, since the baleen whales which Wagner studied feed on small Crustacea which contain hardly any carotene but large quantities of astaxanthin. Astaxanthin is a carotenoid pigment characteristic of marine invertebrates, contains 4 oxygen atoms in the molecule, and does not serve as a vitamin A precursor to warm-blooded animals. On re-investigating the problem we found, in fact, hardly any carotene in the stomach contents of whales or in the euphausiid shrimps on which they feed but, to our surprise, appreciable quantities of preformed vitamin A in both (Kon & Thompson 1949). This first demonstration was by the Carr-Price colour test with antimony trichloride, and though the reaction was perfectly normal we, of course, wished to confirm by biological tests that we were really dealing with vitamin A in a class of animals in which it was not known at the time to be of normal occurrence.

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