OPHTHALMIA ASSOCIATED WITH A DIETARY DEFICIENCY IN FAT SOLUBLE VITAMIN (A)

1921 ◽  
Vol 76 (14) ◽  
pp. 908 ◽  
Keyword(s):  
Vitamin A ◽  
Dietary Deficiency

ULTRAVIOLET LIGHT-ENHANCED VISUALIZATION OF CUTANEOUS SIGNS OF CAROTENE AND VITAMIN A DIETARY DEFICIENCY

2004 ◽  
Vol 59 (2) ◽  
pp. 97-101 ◽  
Author(s):  
E. Uhoda ◽  
L. Petit ◽  
C. Piérard-Franchimont ◽  
G.E. Piérard
Keyword(s):  
Vitamin A ◽  
Ultraviolet Light ◽  
Dietary Deficiency

scholarly journals STUDIES ON EXPERIMENTAL RICKETS

1925 ◽  
Vol 42 (6) ◽  
pp. 793-798 ◽  
Author(s):  
R. Kawamura ◽  
Y. Kasama
Keyword(s):  
Vitamin A ◽  
Egg Yolk ◽  
Vitamin B ◽  
Low Grade ◽  
Phosphorus Metabolism ◽  
Similar Disease ◽  
Vigorous Growth ◽  
Calcium And Phosphorus ◽  
Dietary Deficiency

Our observations show that young rabbits born of mothers afflicted with Schistosomum japonicum develop typical rickets. Rickets can also be produced if we infect the young, healthy rabbits with the same parasite. It is natural to suppose that the rachitic changes are caused by the parasite itself. Since, however, a similar disease can be produced in the offspring, when the mother is fed on egg yolk, the causation is not limited to the action of this parasitic toxin alone. The toxin of Schistosoma may disturb the calcium and phosphorus metabolism of bone in young animals, especially in the period of vigorous growth; that is, 20 to 40 days after birth of the rabbits. Or it may exhaust some element important in the calcium and phosphorus metabolism such as vitamin A or D. The fact that exhaustion of the antirachitic factor in the mother causes rickets in the young, as Grant (1924) showed, and that certain low grade infections can exhaust vitamin B as shown by Wedgewood (1924), is in line with this conception. It may be added here that most investigations on rickets have been carried out on rats and dogs. We have found a simple and excellent way of producing rickets in rabbits by dietary deficiency. Concerning this method, we shall report elsewhere.

Dark Adaptation and Dietary Deficiency in Vitamin A*†

1940 ◽  
Vol 23 (12) ◽  
pp. 1325-1340 ◽  
Author(s):  
Lincoln F. Steffens ◽  
Hugo L. Bair ◽  
Charles Sheard
Keyword(s):  
Vitamin A ◽  
Dark Adaptation ◽  
Dietary Deficiency

Photoreceptor thresholds and visual pigment levels in normal and vitamin A-deprived Xenopus tadpoles

1976 ◽  
Vol 39 (6) ◽  
pp. 1272-1287 ◽  
Author(s):  
P. Witkovsky ◽  
E. Gallin ◽  
J. G. Hollyfield ◽  
H. Ripps ◽  
C. D. Bridges
Keyword(s):  
Vitamin A ◽  
Visual Pigment ◽  
Structural Integrity ◽  
Absolute Threshold ◽  
Normal Diet ◽  
Rod Outer Segments ◽  
Sensitivity Functions ◽  
Outer Segments ◽  
Piii Component ◽  
Dietary Deficiency

1. Measurements of the aspartate-isolated PIII component of the electroretinogram (ERG) were used to estimate photoreceptor threshold in dark-adapted tadpoles of the clawed toad, Xenopus laevis raised on a normal diet. Spectral sensitivity functions established that the rod mechanism governed absolute dark thresholds from stage 40 to the end of premetamorphic development. 2. Parallel measures of rod outer-segment dimensions and visual pigment levels demonstrated a) that visual pigment concentration remained constant at all tadpole stages, and b) that the fall in threshold over the course of premetamorphic development depended exclusively on the increased probability of quantal absorption that accompanied the growth of the rod outer segments. 3. When tadpoles were obtained from vitamin A-deficient females and raised subsequently on a vitamin A-free diet, the first appearance of the ERG was delayed and its absolute threshold raised, with respect to controls. 4. Histological examination of vitamin A-deprived retinas indicated that rod outer segments retained their structural integrity in spite of up to a 75% loss of visual pigment. 5. The threshold rise which accompanied a fall in visual pigment levels, whether effected by dietary deficiency or by bleaching, was greater than could be attributed solely to a reduction in the probability of quantal absorption.

The Morphology of Vacuolated Cells in the Liver Following Administration of Vitamin A.

1973 ◽  
Vol 31 ◽  
pp. 408-409
Author(s):  
Odell T. Minick ◽  
Hidejiro Yokoo ◽  
Fawzia Batti
Keyword(s):  
Electron Microscopy ◽  
Body Weight ◽  
Vitamin A ◽  
Light And Electron Microscopy ◽  
Liver Cells ◽  
Prominent Feature ◽  
Vascular Space ◽  
Vacuolated Cell ◽  
Vacuolated Cells ◽  
Vacuolated Cytoplasm

Vacuolated cells in the liver of young rats were studied by light and electron microscopy following the administration of vitamin A (200 units per gram of body weight). Their characteristics were compared with similar cells found in untreated animals.In rats given vitamin A, cells with vacuolated cytoplasm were a prominent feature. These cells were found mostly in a perisinusoidal location, although some appeared to be in between liver cells (Fig. 1). Electron microscopy confirmed their location in Disse's space adjacent to the sinusoid and in recesses between liver cells. Some appeared to be bordering the lumen of the sinusoid, but careful observation usually revealed a tenuous endothelial process separating the vacuolated cell from the vascular space. In appropriate sections, fenestrations in the thin endothelial processes were noted (Fig. 2, arrow).

The Effect of Vitamin A on the Intermittent Nitrogen Dioxide Gas Exposure in Hamsters

1976 ◽  
Vol 34 ◽  
pp. 176-177
Author(s):  
J.C.S. Kim ◽  
M.G. Jourden ◽  
E.S. Carlisle
Keyword(s):  
Electron Microscopy ◽  
Vitamin A ◽  
Nitrogen Dioxide ◽  
Chronic Exposure ◽  
Light And Electron Microscopy ◽  
Specific Effect ◽  
Deficient Diet ◽  
Intermittent Exposure ◽  
Hypovitaminosis A ◽  
Gas Exposure

Chronic exposure to nitrogen dioxide in rodents has shown that injury reaches a maximum after 24 hours, and a reparative adaptive phase follows (1). Damage occurring in the terminal bronchioles and proximal portions of the alveolar ducts in rats has been extensively studied by both light and electron microscopy (1).The present study was undertaken to compare the response of lung tissue to intermittent exposure to 10 ppm of nitrogen dioxide gas for 4 hours per week, while the hamsters were on a vitamin A deficient diet. Ultrastructural observations made from lung tissues obtained from non-gas exposed, hypovitaminosis A animals and gas exposed animals fed a regular commercially prepared diet have been compared to elucidate the specific effect of vitamin A on nitrogen dioxide gas exposure. The interaction occurring between vitamin A and nitrogen dioxide gas has not previously been investigated.

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