The production of experimental vitamin A deficiency in rats and mice

1971 ◽  
Vol 5 (2) ◽  
pp. 239-250 ◽  
Author(s):  
T. Moore ◽  
P. D. Holmes
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
White Flour ◽  
Short Notice ◽  
Pelleted Diet ◽  
Vitamin A Acid ◽  
Rats And Mice ◽  
Deficient Mice ◽  
Timely Treatment

Vitamin A deficiency in rats and mice was induced by restricting dams and litters from parturition to a pelleted diet made mainly from white flour. Young rats usually developed clear signs of avitaminosis A within 60 days from birth. Mice were more resistant, and some survived for periods up to 150 days from birth. Retention of traces of vitamin A in the liver was no more prolonged in mice than in rats. In mice, enlargement of the prostates and seminal vesicles, and atrophy of the testes, were usually the most prominent pathological features. In rats, timely treatment with vitamin A acid (retinoic acid) cured xerophthalmia and restored growth. Signs of deficiency reappeared soon after its administration was stopped. This procedure allows supplies of animals to be kept in good general health, but ready for the production of acute deficiency at short notice. Retinoic acid was also effective in curing deficient mice. Incidental observations on the eyes and reproductive powers of mice or rats dosed with retinoic acid, and on the response of rats to variations in the casein contents of their diet, are recorded.

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.

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

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.

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.

Vitamin A alters the internal viscosity of fragments of limb-bud mesenchyme

Development ◽  
1980 ◽  
Vol 59 (1) ◽  
pp. 325-339
Author(s):  
T. E. Kwasigroch ◽  
D. M. Kochhar
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Mesenchymal Cells ◽  
Limb Bud ◽  
Mouse Limb ◽  
Vitamin A Acid ◽  
Internal Viscosity ◽  
Fusion Experiments

Two techniques were used to examine the effect of vitamin A compounds (vitamin A acid = retinoic acid and vitamin A acetate) upon the relative strengths of adhesion among mouse limb-bud mesenchymal cells. Treatment with retinoic acid in vivo and with vitamin A acetate in vitro reduced the rate at which the fragments of mesenchyme rounded-up when cultured on a non-adhesive substratum, but these compounds did not alter the behavior of tissues tested in fragment-fusion experiments. These conflicting results indicate that the two tests measure different activities of cells and suggest that treatment with vitamin A alters the property(ies) of cells which regulate the internal viscosity of tissues.

Sign in / Sign up

Export Citation Format

Share Document