Effects of retinoic acid on the concentrations of radioactive metabolites of retinol in tissues of rats maintained on a retinol-deficient diet
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The effect of feeding retinoic acid for 2 and 6 days on the metabolism of labeled retinol in tissues of rats maintained on a vitamin A deficient diet was studied. The metabolites of retinol were analyzed by high performance liquid chromatography. Feeding retinoic acid for 2 days significantly reduced the blood retinol and retinyl ester levels without affecting the vitamin A content of the liver. In intestine and testis the content of labeled retinoic acid was decreased significantly by dietary retinoic acid. Addition of retinoic acid to the diet for 6 days resulted, in addition to decreased blood retinol and retinyl ester values, in an increase in the retinyl ester values in the liver. The accumulation of retinyl ester in the retinoic acid fed rat liver was accompanied by an absence of labeled retinoic acid. Kidney tissue was found to contain the highest levels of labeled retinoic acid, retinol, and retinyl esters; dietary retinoic acid did not alter the concentrations of these retinoids in the kidney during the experimental period. Since kidney retained more vitamin A when the liver vitamin A was low and also dietary retinoic acid did not affect the concentrations of radioactive retinoic acid in the kidney, it is suggested that the kidney may play a major role in the production of retinoic acid from retinol in the body.Key words: retinol, retinoic acid, vitamin A deficiency, tissue metabolites, rat.Keywords:
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The effects were comparcd on mouse tail scale epidermis of vitamin A acid, acetate and alcohol (all as the trans isomer) and the cis aldehyde by regular topical applications. Increases in epidermal thickness produced by different doses were compared statistically, and the induction of a granular layer and of epidermal alkaline phosphatase activity was demonstrated. The different forms and isomers of vitamin A have similar effects on the epidermis, but vary individually in activity, Retinoic acid and trans‐retinyl acetate were very similar in their action when used in a water solubilizing vehicle. The fact that retinyl acetate is very much cheaper than retinoic acid is a point in favour of its use for the treatment of psoriasis.
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The relationship between dietary vitamin A and all-trans-retinoic acid levels in serum and tissues had not been quantified. We determined the impact of dietary vitamin A on retinoid levels in serum, liver, kidney, testis, and epididymal white adipose of five mouse strains: AKR/J; BALB/cByJ; C3H/HeJ; C57BL/6J; 129S1/SvImJ. Retinoids were quantified in mice fed copious vitamin A (lab chow, ≥20 IU/g) followed by one month feeding a vitamin A-sufficient diet (4 IU/g), or after three generations of feeding a vitamin A-sufficient diet. Retinol and retinyl esters were measured by high-performance liquid chromatography with ultraviolet absorbance detection. All-trans-retinoic acid was quantified by liquid chromatography tandem mass spectrometry. The amounts of dietary vitamin A had long-term strain-specific effects on tissue retinyl ester, retinol and all-trans-retinoic acid concentrations. Three generations of feeding a vitamin A-sufficient diet decreased all-trans-retinoic acid in most tissues of most strains, in some cases more than 60%, compared to a diet with copious vitamin A. With both diets, all-trans-retinoic acid concentrations maintained an order of liver ≈ testis > kidney > white adipose tissue ≈ serum. Neither retinol nor all-trans-retinoic acid in serum reflected all-trans-retinoic acid concentrations in tissues. Strain and tissue-specific differences in retinol and all-trans-retinoic acid altered by different amounts of dietary vitamin A could have profound effects on retinoid action. This would be the case especially with the increased all-trans-retinoic acid values associated with the amounts of vitamin A and its precursors (carotenoids) in chow diets.
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1. Male and female chickens were reared from hatching on vitamin A-free diets, either unsupplemented or containing retinoic acid (vitamin A acid), methyl retinoate or retinyl acetate (vitamin A acetate). The birds given retinyl acetate grew well and had a normal appearance, but those given the unsupplemented diet died before 4 weeks of age after developing typical signs of avitaminosis A. The birds given retinoic acid or methyl retinoate did not show overt signs of vitamin A deficiency or other abnormalities except for a progressive failure of vision. Minimal histological changes were found in their retinas, and their vision was rapidly restored after feeding with retinyl acetate. 2. The cocks maintained with retinoic acid or methyl retinoate had normal testes and the hens laid eggs at a normal rate, but although their eggs could be obtained fertile the development of the embryo became abnormal after 2 days incubation and it always died. The development of the embryos could be stimulated and sometimes restored to normal by injection of various forms of vitamin A into the eggs before incubation, or by previous administration of retinyl acetate to the hens. 3. It is concluded that feeding retinoic acid as the sole source of vitamin A enables the hen to produce eggs that lack vitamin A but are otherwise normal, thus permitting the demonstration of a hitherto undescribed requirement of the early chick embryo for vitamin A. 4. The toxicity of vitamin A derivatives to chick embryos was investigated; injected retinoic acid was found to be extremely toxic.
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Content of retinol, retinyl acetate and retinyl palmitate was studied by means of high pressure liquid chromatography, in liver tissue of mice, kept on a vitamin A-free diet during various periods of time. Cell proliferative activity and formation of specific T-killers were distinctly inhibited in mixed culture of lymphocytes from spleen tissue of A-avitaminous animals. Proliferative and cytolytic activity of the stimulated lymphocytes might be corrected by means of retinoic acid and retinyl acetate in vitro and in vivo.
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