S. H. Rubin

Physicochemical assay of vitamin A and related compounds.

Publisher Summary The substance designated as “vitamin A 2 ” has been isolated from liver oils of freshwater fish, therefore, vitamin A should be called A 1 . This term is used only when the need arises to distinguish between the two substances. There are 16 cis-trans isomers that are possible in a molecule with four double bonds in the side chain; six of these isomers have been prepared to date in a pure state. This chapter discusses only with principles of analysis of vitamin A and of related substances. The all-trans form of vitamin A is the one most widely found among the cis-trans isomers. It has the highest biological activity and is used as the International Standard. The known cis-trans isomers among the 16 that are theoretically possible are listed in this chapter. There are, according to Pauling, 12 sterically hindered and 4 unhindered cis-trans isomers. All the unhindered isomers are known: all-trans, neo-a, iso-a, and iso-b. Neo-b and neo-c are hindered isomers. Methods for the quantitative isolation and determination of the isomers in mixtures would be of great interest because of differences in the biological activity of the isomers.

Vitamin a Requirements of Animal Species

Publisher Summary In considering the requirement of an animal for a vitamin, a prime question concerns the criteria to be used. In general, the minimum requirement of a species for vitamin A has been considered to be that level, which gives satisfactory growth and prevents lesions or dysfunctions because of vitamin A deficiency. This is, perhaps, a somewhat arbitrary standard, which does not consider other important factors influenced by vitamin A intake: tooth development, longevity, and maintenance of adequate liver stores and blood levels of vitamin A, particularly during pregnancy and lactation. The amount of vitamin A required to provide optimal conditions with regard to these latter considerations may be widely different from the minimum requirement established on the usual basis noted above. In other words, the daily intake needed to correct or prevent a frank clinical deficiency may be quite different from the amount necessary to correct or prevent a deficiency the existence of which can be elicited only by examination with special means or by special analyses.

Urinary Excretion of Hydrazine Derivatives of Isonicotinic Acid in Normal Humans

Summary Urinary excretions after oral dosage of Rimifon and Marsilid to 9 normal humans have been studied colorimetrically by means of the reaction with 10% cyanogen bromide in ammonia buffer. The influence of non-specific chromogens has been eliminated to a large degree by parallel, assays of pre-dosage control urines. The concentration of metabolite in which the hydrazide linkage has been split was determined by direct assay and the results expressed as “free isonicotinic acid” pending positive identification. The increase in colorimetric readings upon permanganate treatment has been ascribed to unchanged Rimifon or Marsilid, although, again, the exact nature of these excretion products has not been ascertained. Total excretions in 48 hours average about 65% of the dose of both Rimifon and Marsilid, but in the same period the excretion of unhydrolyzed Marsilid is only about half that of Rimifon. In the first few hours after dose, the relative rate of excretion of Marsilid is still lower, averaging only about one-fourth that of Rimifon. Approximately half of the Rimifon is split prior to excretion and almost identical excretion patterns are found at the 192 and 125 mg dose levels. In case of Marsilid, the excretion of free isonicotinic acid parallels closely its excretion after Rimifon for 8 hours, but the 24- and 48-hour totals of free isonicotinic acid are about 50% higher after Marsilid. This increased excretion of the split product results apparently from the longer retention of Marsilid in the body.

A critique of biological activity of L-lyxoflavin.

Summary Lyxoflavin has been shown to possess a limited ability to replace riboflavin in the nutrition of L. casei and the rat. In chicks, large doses of lyxoflavin produce small weight gains, which, however, can be matched by equal doses of riboflavin. The present evidence does not warrant the classification of lyxoflavin as a new vitamin.

Utilization of d-biotinol by microorganisms, the rat and human.

Summary d-Biotinol does not replace d-biotin in the nutrition of L. arabinosus, L. casei, or S. cerevisiae but is fully as effectiveas d-ibiotin in curing egg white-induced bio tin deficiency in the rat. Comparison of urinary excretions of biotin after oral or intramuscular administration of biotin and biotinol shows the latter to be converted to biotin efficiently by both rat and human.

Effect of niacin and tryptophan in counteracting toxicity of crystalline borrelidin for rat.

Conclusions When crystalline borrelidin is given orally to rats at a level of 10 μg per day, poor growth results. This inhibition of growth can be partially overcome by supplementation with niacin. Two μg of borrelidin per day given orally is without effect upon the growth of rats whereas 20 μg per day results in a high mortality rate. Poor growth is also observed in rats receiving a basal ration containing levels of 1 and 2 mg borrelidin per kilo. The addition of niacin or tryptophan results in significantly better growth.

Effect of Long-Term Panthenol Administration on the Pantothenate and Coenzyme A Contents of Rat Tissues.

Summary Toxicity tests of panthenol show that this biologically active, hydroxy analogue of pantothenic acid has no in vivo antivitamin effect in mammals. In acute toxicity tests, mice tolerated up to 6.25 g per kilo and rabbits up to 3 g per kilo. In chronic feeding tests, 2 mg per day of panthenol had no inhibitory effect upon the growth rate of normal rats on an adequate stock diet and 20 or 500 mg daily produced no histopathological or hematological changes in rats or dogs, respectively. When fed as above at the 2 mg per day level for periods up to 6 months, panthenol did not differ significantly from an equivalent supplement of calcium pantothenate in its effect on rat tissue storage of pantothenate. Total pantothenate in the liver, spleen, kidney and heart, and coenzyme A in the liver were equal or slightly greater in the dosed groups than in the controls. Liver storage in all groups was almost entirely as coenzyme A, and no appreciable amounts of panthenol or free pantothenate accumulated.