VITAMIN- A

DR.L.KARPAGAVEL
PROFESSOR & HOD
DEPARTMENT OF BIOCHEMISTRY
 DEFINITION
Vitamins are organic substances that are required in small
amounts in diet for optimal health and growth

Usually not synthesized in the humans and should be

supplied in the diet

Micronutrients

Do not provide energy, but they take part in metabolic

reactions of macro nutrients that release energy

Classified as fat soluble and water soluble

Fat soluble vitamins Water soluble vitamins

Lipid soluble Water soluble

Mostly isoprenoid Heterogeneous

compounds
Not readily excreted in Easily excreted
urine
Excess can lead to No toxicity
accumulation & toxicity

Stored in liver Not stored except B12

 PROGRESS OF SESSION
INTRODUCTION

CHEMISTRY& STRUCTURE

ABSORPTION,STORAGE&TRANSPORT

DIETARY SOURCES & RDA

MECHANISM OF ACTION

BIOCHEMICAL FUNCTIONS

DEFICIENCY MANIFESTATIONS

TOXICITY
 INTRODUCTION
One of the Common vitamin
clinically used

Treatment of Acne, Post-

inflammatory scar
(inhibits inflammation,
keratinization,decreases sebum
secretion)

Vitamin A skin creams are used to

smooth wrinkles, skin glowing

Combat infections – role in T-

CELL, humoral immunity,NK-
Cells activity
 CHEMISTRY
Vitamin A occurs in two forms in food ( RETINOIDS & CAROTENOIDS)
RETINOIDS CAROTENOIDS
Animal origin Plant origin
Retinol, Retinal & Retinoic β carotene
acid

20 c, one ß ionone 40c, two ß ionone ring

ring

Preformed vitamin
Pro vitamin
 STRUCTURE
Common
• β ionone ring
• Unsaturated side chain (polyisoprene)
Retinol: Terminal alcohol

Retinal: Terminal aldehyde

Retinoic acid: Carboxylic acid.

β carotene: 2 Retinal linked
together
ABSORPTION &STORAGE &TRANSPORT
POINTS TO REMEMBER IN ABSORPTION &STORAGE
&TRANSPORT

•Retinyl esters present in the diet are converted to retinol and absorbed

•β carotene in the diet absorbed as itself and then converted to retinol

•Occurs at the level of upper small intestine and requires bile salt.

•In the intestinal mucosal cells it is re-esterified and transported to liver

through chylomicron.

•Stored as retinol palmitate in Stellate cells of Liver.

•From liver to target cells it is transported complexed with retinol

binding protein.
 DIETARY SOURCES

FISH LIVER OIL, EGG YOLK, MILK & DAIRY PRODUCTS

CARROTS,PAPAYA,MANGO
 RDA

Men -750-1000µg/day
Women -750µg/day
Pregnancy -1000µg/day
Lactation -1200µg/day
 MECHANISM OF ACTION
Receptors – INTRACELLUAR Nuclear receptor ,resembles
steroid

Retinol- Retinol binding protein (RBP) complex reaches target

tissue.

Retinol enters inside the cell.

Cellular retinoic acid binding protein(CRBP)

Hormone response elements (HRE) of DNA

Regulates Gene Expression for proteins

 BIOCHEMICAL FUNCTIONS OF VITAMIN-A

Retinol- Normal Reproductive function

Retinal- Normal Vision

Retin oic acid- Regulation of Gene Expression- Growth &
differentiation
β carotene- Antioxidant

- Maintenance of Normal epithelium

- Differentiation of Immune system cells
 VISION: ROLE OF RETINAL

Rods for Dim vision – contain rhodopsin (11-cis retinal

+opsin)
Cones for Color vision – contains Conopsin

Rhodopsin cycle : comprises two distinct events

1. Bleaching of rhodopsin and generation of nerve impulse

2. Regeneration of rhodopsin
 BLEACHING OF RHODOPSIN AND GENERATION OF NERVE IMPULSE

Series of Photo isomerisation reaction takes place leading to generation

of nerve impulse
PATHWAY FOR GENERATION OF NERVE IMPULSE

Activation of transducin
↓

Increased conversion of cGMP to GMP

↓
Decrease in cGMP
↓
Closure of sodium channel
↓
hyper polarization
↓
Generation of nerve impulse
WALD’S VISUAL CYCLE- REGENERATION OF RHODOPSIN

R
E
T
I
N
A 1)

2)
2 PATHWAYS FOR REGENERATION OF 11 CIS-RETINAL

1) TRANS -RETINOL DIRECTLY ISOMERIZED TO CIS FORM

IN THE RETINA ITSELF

2) TRANSPORED TO LIVER - FIRST REDUCED,THEN

ISOMERIZED AND THE OXIDISED TO CIS -RETINAL
 DEFICIENCY MANIFESTATIONS

EYE MANIFESTATIONS (LINE BECK)

1.Loss of sensitivity to green light -

Earliest
2.Increased Dark adaptation time
3.Night Blindness (Nyctalopia)
4.Xerophthalmia-Dry eye
5.Bitot’s spot
6.Keratomalacia-Softening of the cornea
7.Corneal ulcer
8. Keep Away Blindness
 ? ALL THESE LESIONS

1. Impaired epithelial cell differentiation

Vitamin A is essential for the normal differentiation of
epithelial cells, the cells that make up the conjunctiva and
cornea. In a deficiency of vitamin A, these cells are unable to
differentiate properly, which leads to the formation of abnormal
cells that are more susceptible to damage.

2. Reduced tear production:

Vitamin A is also important for the production of tears, which
help to keep the eye moist and protect it from infection. In a
deficiency of vitamin A, tear production is reduced, which can lead
to the drying and inflammation of the eye.
 OTHER MANIFESTATIONS
GROWTH RETARDATION:
Failure of skeletal growth
Defective synthesis of chondroitin sulphate

SKIN
Follicular Hyper keratosis (or) Phrynoderma, Acne

IMMUNE SYSTEM- IMPAIRED

Keratinisation of the mucosal cells of the Respiratory, GIT and

Genito urinary tract

More susceptible to recurrent infections

 THERAPEUTIC USES
All Trans’ retinoic acid (Tretinoin)
1.PSORIASIS
2.PROMYELOCYTIC LEUKEMIA
3.ACNE

PSORIASIS
ACNE
 VITAMIN A TOXICITY
:

Vitamin A is highly toxic when taken in large amounts either

acutely or chronically
Unbound Vit A causes tissue damage

CNS Manifestation-Increased Intra Cranial Tension

Signs include headache, nausea and vomiting, increased
cerebrospinal fluid pressure, blurred vision ,dry & peeling skin

Excess Vitamin A in Pregnancy is Teratogenic

SUMMARY
THANKYOU