Vitamin A( Animals and HUmans)

This slide deals with different aspects of vitamin A sources, their deficiency syndromes particularly in Animals

1. Welcome to presentation Vitamin A

2. Overview Vitamin A occurs as retinol, retinoic acid, and retinal. It is a fat-soluble compound . Together with its precursors, the carotenoids, it is highly labile and rapidly destroyed by light , oxygen, heat, and acid.

3. Overview Vitamin A is required by all mammals and is synthesized through the metabolism of carotenoid precursors (carotenes) present in Leaves and some grains.

4. Absorption The proximal jejunum is the primary site of vitamin A and carotene absorption. A normal pancreatic, hepatic, and biliary function, together with an adequate dietary fat content and normal fat digestion and absorption, is required for the absorption of β-carotene and its subsequent conversion to retinol. Ruminal microbial degradation of biologically active vitamin A is appreciable and varies with diet composition.

5. sources

6. Transport Transported via chylomicrons from intestinal cells to liver. Transported to targeted tissue from liver as a retinol through retinol binding protein, which is bind as transthyretin .

7. Storage Liver is main storehouse. Stored as retinopalmitate EXCEATION Not readily excreted Execrated via urine .

8. Factors affecting vitamin A utilization Environmental temperature : high temperature leads to utilization of vitamin a Ration : higher concentrate feed leads to higher metabolism and leads to higher utization of vitamin a ,and High-concentrate diets can result in up to 70 % pre-intestinal degradation of vitamin A, whereas diets with > 75% forage result in < 20 % degradation, factors to be taken into account for diet formulation and vitamin A or β- carotene supplementation Hypothyroidism :thyroxin it helps in conversion of carotene to vitamin a . Hypophostaemia : low phosphorus levels retards the conversion of carotene to vitamin a.

9. Cathartic drug : oligenous purgatives (liquid paraffin )decreased the availability of vitamin through excretion from gut as the vitamin is fat soluble . Nitrates and Nitrites :interfere the conversion of vitamin carotene to vitamin A

10. General functions Vitamin A is required for cellular differentiation , growth and development adequate vision, thyroid gland function, protein synthesis , conversion of cholesterol to corticosterone, glycogen synthesis, Immune function, regulation of gene expression,and iron metabolism

11. Deficiency Growth : causes poor appetite and emaciation in growing animals . Vision : ocular signs primary secondary

12. Primary signs : Conjunctival xerosis Corneal xerosis Corneal ulceration Keratomalacia Secondary signs Night blindness Xeropthalmia Corneal scar

13. Keratomalacia A softening and ulceration of the cornea of the eye resulting from severe systemic deficiency of vitamin A.

14. Night Blindness ( Nyctalopia )

15. Neurologic disorder Limb weakness Incoordination and paralysis of skeletal muscle . Facial paralysis Rotation of head

16. Congenital Anamolies Anophthalmos Cleft plate Microphthalmos

17. Bone development

18. Mucus epithelial cells Deficiency of vitamin A Loss of integrity of epithelial cells Secretary cells are transformed to keratinized cells Inefficient synthesis of mucopolysacchrides

19. Epithellial cells Skin :hyper keratinization of skin lead to xerodermia Alimentary tract :degenerative changes to intestinal epithelium and secretory glands. Respiratory tract : degenerative changes and stratification of epithelium. Urinary system :degeneration and cornification of epithelium Reproduction :impaired oogenesis and spermatogenesis leads to reproductive failure

20. Toxicity osteoporosis , reduced feed intake decreased cerebrospinal fluid pressure . skeletal malformation and osteoporosis leading to spontaneous fractures, anemia, delayed blood clotting and internal hemorrhages , partial or total anorexia, growth retardation and weight loss, alopecia . Skin thickening with hyperkeratosis enteritis with chronic diarrhea, hepatomegaly and splenomegaly with degenerative atrophy and fatty infiltration of liver and kidneys, conjunctivitis, and congenital abnormalities.

21. CAUSES AND RISK FACTORS Poor dietary formulation with low or excessive vitamin A and/or inadequate fat content. Low forage availability . Feed exposure to light and heat or the presence of moisture and trace minerals accelerates the loss of vitamin A activity.

22. DIFFERENTIAL DIAGNOSES Deficiency Cattle : Polioencephalomalacia , lead poisoning, water deprivation/sodium toxicosis , meningoencephalitis . other causes of increased intracranial pressure and blindness . Small ruminants: Pregnancy toxemia and listeriosis .

23. Toxicity All causes of skeletal malformations and spontaneous fractures, hepatic lipidosis , and renal failure

24. Treatment Deficiency is rapidly corrected with vitamin A supplementation (dietary and injectable ). Common dietary sources of carotenes are carrots, yellow corn, alfalfa (legumes), green grass (pasture, hay, or silage ). Advanced clinical signs of both deficiency and toxicity are irreversible.