Vitamin A what forms do they exist in.
RDA
VITAMIN A, exists in;
1. Alcoholic- Retinol
2. Aldehyde- Retinal
3. Acid- Retinoic acid
[collectively called RETINOIDS]
Pro-vitamin A(CAROTENOIDS):
alpha carotene, beta carotene
Dietary allowance;
Adults: 5000UI, higher in childrens, pregnant lactating women.
Vitamin A composition/importance
Rods for dim light vision
Cones for bright light vision.
Rod cells contain rhodopsin(visual pigment);
opsin protein part.
retinene non protein part.
[rhodopsin absorbs light and splits into cis/trans]
Sources of Vitamin A
LIVER, Milk, Cheese, Egg yolk
Which form of Vitamin A is involved in gene expression
Retinoic acid
Importance of Vitamin A
Vision
Role in reproduction
Maintenance of skin
role in cell division
role in bone construction
Toxicity from Vitamin A
Excessive intake produces a toxic syndrome called HYPERVITAMINOSIS A
signs and symptoms:
CNS: headache,nausea
Skin: Dry, Alopecia
VITAMIN D types
RDA
D-3 or Cholicalciferol, produced in skin.
Inactive natural precursors of V-D are PRO-VITAMINS.
1. Ergosterol: D2 found in plants
2. 7-dehydrocholestrol: D3 found in skin
RDA:
(adult) 400IU
pregnant mother: 600IU
Sources of Vitamin D
Fish, liver oil, egg yolk, Marganine.
7 dehydrocholestrol is formed cholestrol in the intestinal mucosa and principally liver passed on the skin where it undergoes activation to vitamin D3 by the action of solar UV rays
primary function(s) of Vitamin D
MAINTAINS CALCIUM
- Increasing absorption of calcium by intestine.
- minimizing loss of calcium by kidney
- Reabsorption (demineralisation) of bone when necessary
Diseases and toxicity Vitamin D
deficiency causes:
DEmineralization of bones causing Rickets in children, osteomalacia in adults.(Hypocalcemia)
Toxicity:
Excessive intake produces toxic syndrome called HYPERVITAMOSIS-D.
Higher calcium(Hypercalcemia), nausea, kidney damage.
(if taken 500x-1000x normal req)
Vitamin E
Fat soluble antioxidant.
includes tocopherols and toco trienols.
.Essential for maintaining cell integrity
.Protects cell membrane ftom oxidative damage [Anti-oxidant]
Vitamin E sources
- vegetable oils(sunflower,wheat germ)
- Nuts and seeds(sunflower seeds)
- Fortified cereals
- Green leafy veggies
Vitamin E Absorption & Transport
- Absorbed in small intestine with fats
- Requires bile salts for emulsification
- incorporated into chylomicrons
- Transported via Lymphatics to circulation
Vitamin E metabolism and storage
Transported to liver
Stored in adipose tissue and liver
Alpha-tocopherol prefentially retained
Excess metabolised & excreted
Fat soluble vitamins
Vitamin A, D, E, K
Vitamin E functions
powerful antioxidant
prevents lipid peroxidation
protects RBC membranes
supports immune function
maintains neurological identity
Vitamin E deficiency
very rare seen in FAT MALABSORPTION
Hemolytic anemia
Muscle weakness
Peripheral neuropathy
Retinopathy
Vitamin E toxicity
Clinically important.
Rare but high doses can cause bleeding.
Interferes with Vitamin K function
MAY INCREASE RISK OF HEMORRHAGE
Vitamin E RDA
15mg/day
increased needs in oxidative stress conditions
Vitamin K
fat soluble essential for coagulation.
Includes K1(phyloquinone) from leafy greens
and K2(menaquinone) from fermented foods, animal products
Critical for SYNTHESIS if clotting factors, or POST TRANSLATIONAL modification of clotting factors
Vitamin K sources
Green leafy veggies (Spinach, kale)
Gut microbiota synthesis (K2/menaquinone)
Vitamin K absorption
Absorbed in small intestine
requires bile salts
Transported in chylomicrons
(then into systemic circulation)
Stored in liver
Vitamin K metabolism
undergoes vitamin k cycle,
where its oxidised &
converted bw active and inactive forms.
Recycled in Liver
[WARFARIN(anticoagulant) inhibits the cycle]
Vitamin K functions
Activation of clotting factors 2,7,9,10
activation of anticoagulant proteins, Protein C and protein S
Rone in bone metabolism(osteocalcin)
Prevents bleeding.
