Biological Activity of Retinoic Acid Ester in the Domestic Fowl : Production of Vitamin A Deficiency in the Early Chick Embryo

Nature ◽  
1965 ◽  
Vol 205 (4975) ◽  
pp. 1006-1007 ◽  
Author(s):  
J. N. THOMPSON ◽  
J. McC. HOWELL ◽  
G. A. J. PITT ◽  
CATHERINE I. HOUGHTON
Keyword(s):  
Biological Activity ◽  
Retinoic Acid ◽  
Chick Embryo ◽  
Vitamin A ◽  
Acid Ester ◽  
Domestic Fowl ◽  
Vitamin A Deficiency ◽  
Early Chick Embryo

scholarly journals The uptake and metabolism of retinol, retinoic acid and methyl retinoate by the early chick embryo

1969 ◽  
Vol 23 (4) ◽  
pp. 899-904 ◽  
Author(s):  
B. Morgan ◽  
J. N. Thompson ◽  
G. A. J. Pitt
Keyword(s):  
Retinoic Acid ◽  
Chick Embryo ◽  
Vitamin A ◽  
Early Embryo ◽  
Radioactive Substance ◽  
Chain Fatty Acid ◽  
Long Chain Fatty Acid ◽  
Early Chick Embryo ◽  
Uptake And Metabolism ◽  
Very High

1. Fertile eggs deficient in vitamin A were obtained by feeding hens a diet deficient in retinol (vitamin A alcohol) but containing methyl retinoate.2. Radioactive retinol was injected into the albumen of three of these eggs at a level of 2 μg [6,7-14C]retinol/egg. After 5 days' incubation, 4.6–8.3% of the injected material was recovered in the lipid of the embryo, representing a four- to nine-fold concentration into the embryo from the albumen. Approximately 40–50% of this was unchanged retinol, 15–20% retin-aldehyde and 20–30% probably a long-chain fatty acid retinyl ester. The early embryo can, therefore, metabolize vitamin A very effectively.3. [6,7-14C]Retinoic acid (2 μg) was injected into normal fertile eggs, killing most of the embryos. The eggs with dead embryos were analysed; 0.24% and 0.33% of the injected material was recovered from the embryos. Two embryos which developed contained 0.51% and 0.53% of the injected dose. In no instance was any material identified other than retinoic acid. The extremely low amounts of retinoic acid absorbed by the embryos emphasize the very high toxicity of retinoic acid to the early chick embryo.4. [6,7-14C]Methyl retinoate (0.5 μg) was injected into each of four normal eggs; 8.5–11.6% was isolated as unchanged methyl retinoate after 5 days; no other radioactive substance was detected.

scholarly journals The biological activity of retinoic acid in the domestic fowl and the effects of vitamin A deficiency on the chick embryo

1969 ◽  
Vol 23 (3) ◽  
pp. 471-490 ◽  
Author(s):  
J. N. Thampson ◽  
J. McC. Howell ◽  
G. A. J. Pitt ◽  
Catherine I. McLaughlin
Keyword(s):  
Retinoic Acid ◽  
Chick Embryo ◽  
Vitamin A ◽  
Progressive Failure ◽  
Vitamin A Deficiency ◽  
Sole Source ◽  
Retinyl Acetate ◽  
Histological Changes ◽  
Acid Methyl ◽  
Vitamin A Acid

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.

Complex regulation of TGF beta expression by retinoic acid in the vitamin A-deficient rat

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 1081-1086 ◽  
Author(s):  
A.B. Glick ◽  
B.K. McCune ◽  
N. Abdulkarem ◽  
K.C. Flanders ◽  
J.A. Lumadue ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Alveolar Epithelium ◽  
Tgf Beta ◽  
Basal Expression ◽  
Beta 2 ◽  
Complex Regulation ◽  
First Time

We report the results of a histochemical study, using polyclonal antipeptide antibodies to the different TGF beta isoforms, which demonstrates that retinoic acid regulates the expression of TGF beta 2 in the vitamin A-deficient rat. Basal expression of TGF beta 2 diminished under conditions of vitamin A deficiency. Treatment with retinoic acid caused a rapid and transient induction of TGF beta 2 and TGF beta 3 in the epidermis, tracheobronchial and alveolar epithelium, and intestinal mucosa. Induction of TGF beta 1 expression was also observed in the epidermis. In contrast to these epithelia, expression of the three TGF beta isoforms increased in vaginal epithelium during vitamin A deficiency, and decreased following systemic administration of retinoic acid. Our results show for the first time the widespread regulation of TGF beta expression by retinoic acid in vivo, and suggest a possible mechanism by which retinoics regulate the functions of both normal and pre-neoplastic epithelia.

scholarly journals A new approach to the assessment of marginal vitamin A deficiency in children in suburban Guwahati, India: hydrolysis of retinoyl glucuronide to retinoic acid

2008 ◽  
Vol 101 (6) ◽  
pp. 794-797 ◽  
Author(s):  
Pulin C. Sarma ◽  
Bhabesh C. Goswami ◽  
Krishna Gogoi ◽  
Harsha Bhattacharjee ◽  
Arun B. Barua
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Serum Retinol ◽  
Serum Samples ◽  
Group I ◽  
High Prevalence ◽  
Hydrolysis Of ◽  
Β Carotene

The objective of the present study was to determine marginal vitamin A deficiency (VAD) by testing the hydrolysis of retinoyl glucuronide (RAG) to retinoic acid (RA) in children. Previous studies in rats showed that hydrolysis occurred when rats were vitamin A deficient. Children (n 61) aged 3–18 years, were divided into two groups, I and II. Blood was collected from the children in Group I (n 19) who were not dosed with RAG. Children in Group II (n 42) were administered all-trans retinoyl glucuronide (RAG) orally, and blood was collected 4 h after the dose. All serum samples were analysed for retinoids and carotenoids. RA was detected in serum only when serum retinol was < 0·85 μmol/l. Thus, hydrolysis of RAG to RA occurred in children with VAD or marginal VAD. Serum retinol was < 0·35 μmol/l in twenty-one children, 0·35–0·7 μmol/l in twenty-three children, 0·7–0·9 μmol/l in eleven children and >1 μmol/l in six children. Mean serum retinol in sixty-one children was 0·522 (sd 0·315) μmol/l. Mean β-carotene (0·016 (sd 0·015) μmol/l) was far below normal compared to the level of lutein (0·176 (sd 0·10) μmol/l) in sixty-one children. A low β-carotene level might be due to a low intake of carotene but high demand for vitamin A. The RAG hydrolysis test may prove to be a useful approach for the determination of marginal VAD with no clinical or subclinical signs of VAD. High prevalence of VAD amongst certain communities in Assam cannot be ruled out.

scholarly journals Role of Vitamin A in Mammary Gland Development and Lactation

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 80 ◽  
Author(s):  
M. Teresa Cabezuelo ◽  
Rosa Zaragozá ◽  
Teresa Barber ◽  
Juan R. Viña
Keyword(s):  
Retinoic Acid ◽  
Mammary Gland ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Retinoid Signaling ◽  
Nutritional Problem ◽  
Pregnancy And Lactation ◽  
Gland Development

Vitamin A (all-trans-retinol), its active derivatives retinal and retinoic acid, and their synthetic analogues constitute the group of retinoids. It is obtained from diet either as preformed vitamin A or as carotenoids. Retinal plays a biological role in vision, but most of the effects of vitamin A are exerted by retinoic acid, which binds to nuclear receptors and regulates gene transcription. Vitamin A deficiency is an important nutritional problem, particularly in the developing world. Retinol and carotenoids from diet during pregnancy and lactation influence their concentration in breast milk, which is important in the long term, not only for the offspring, but also for maternal health. In this study, we review the role of vitamin A in mammary gland metabolism, where retinoid signaling is required not only for morphogenesis and development of the gland and for adequate milk production, but also during the weaning process, when epithelial cell death is coupled with tissue remodeling.

scholarly journals Monitoring Maternal Beta Carotene and Retinol Consumption May Decrease the Incidence of Neurodevelopmental Disorders in Offspring

2011 ◽  
Vol 6 ◽  
pp. CMRH.S8372 ◽  
Author(s):  
Joel S. Goldberg
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Neurodevelopmental Disorders ◽  
Vitamin A Deficiency ◽  
Beta Carotene ◽  
First Trimester ◽  
Trans Retinoic Acid ◽  
First Trimester Of Pregnancy ◽  
Behavioral Teratogen ◽  
Physical And Chemical

Retinoic acids (13-cis and 13-trans) are known teratogens, and their precursor is retinol, a form of vitamin A. In 1995, Rothman et al demonstrated an association between excessive vitamin A, > 10,000 IU/day, during the first trimester of pregnancy and teratogenic effects, particularly in the central nervous system. However, vitamin A deficiency has long been known to be deleterious to the mother and fetus. Therefore, there may be a narrow therapeutic ratio for vitamin A during pregnancy that has not previously been fully appreciated. Neurodevelopmental disorders may not be apparent by macroscopic brain examination or imaging, and proving the existence of a behavioral teratogen is not straightforward. However, an excess of retinoic acid and some neurodevelopmental disorders are both associated with abnormalities in cerebellar morphology. Physical and chemical evidence strongly supports the notion that beta carotene crosses the placenta and is metabolized to retinol. Only very limited amounts of beta carotene are stored in fetal fat cells as evidenced by the fact that maternal fat is yellow from beta carotene, whereas non-brown neonatal fat is white. Furthermore, newborns of carotenemic mothers do not share the yellow complexion of their mothers. The excess 13-trans retinoic acid derived from metabolized beta carotene in the fetus increases the concentration of the more teratogenic 13-cis retinoic acid since the isomerization equilibrium is shifted to the left. Therefore, this paper proposes that consideration be given to monitoring all potential sources of fetal 13-cis and 13-trans retinoic acid, including nutritional supplements, dietary retinol, and beta carotene, particularly in the first trimester of pregnancy.

Vitamin A deficiency in mice causes a systemic expansion of myeloid cells

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3349-3356 ◽  
Author(s):  
Takeshi Kuwata ◽  
I-Ming Wang ◽  
Tomohiko Tamura ◽  
Roshini M. Ponnamperuma ◽  
Rachel Levine ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Cell Population ◽  
Vitamin A Deficiency ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Direct Result ◽  
Essentially Normal ◽  
Deficient Mice

Abstract To examine the role of retinoids in hematopoietic cell growth in vivo, we studied female SENCAR mice made vitamin A deficient by dietary restriction. Deficient mice exhibited a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. The abnormal expansion of myeloid cells was detected from an early stage of vitamin A deficiency and contrasted with essentially normal profiles of T and B lymphocytes. This abnormality was reversed on addition of retinoic acid to the vitamin A–deficient diet, indicating that the myeloid cell expansion is a direct result of retinoic acid deficiency. TUNEL analysis indicated that spontaneous apoptosis, a normal process in the life cycle of myeloid cells, was impaired in vitamin A–deficient mice, which may play a role in the increased myeloid cell population. Quantitative reverse transcriptase-polymerase chain reaction analysis of purified granulocytes showed that expression of not only RAR, but RXRs, 2 nuclear receptors that mediate biologic activities of retinoids, was significantly reduced in cells of deficient mice. This work shows that retinoids critically control the homeostasis of myeloid cell population in vivo and suggests that deficiency in this signaling pathway may contribute to various myeloproliferative disorders.

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