vitamin-a

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VITAMIN - A: 

VITAMIN - A FUNCTIONS ROLE IN VISION: Wald’s Visual Cycle Rhodopsin Cycle GEORGE WALD Cones : Iodopsin Rods : Rhodopsin

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Light waves striking these receptors produce chemical changes which in turngives rise to nerve impulse. Rhodopsin / visual purple is a conjuated protein, containing Opsin as its apoprotein and retinene as its prosthetic froup.

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Retinene in rhodopsin is II – cis retinal. (The aldehyde group of II – cis retinal is bpund to £-NH 2 group of Lys. Of Opsin) Even dimlight can break rhodopsin.

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Walds Visual cycle Rhodopsin Photorhodopsin Bathorhodopsin Lumirhodopsin Metarhodopsin I Metarhodopsin II Metarhodopsin III

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Retinal isomerase All trans retinal II-cis retinal Cis retinal Trans retinal Cis retinal Transretinal Liver Trans retinal Retinolisomerase in lver

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Transducin – GTP Inactive Active Phosphodiesterase Phosphodiesterase CGMP 5’ GMP Na+ channel Na+ channel open (dark) open (in light) hyperpolarisialun generation of nerve impulse Transmited to visual centres in brain

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In dark, there are high level of C- GMP, which binds to the Na+ channels, causing them to open In light, Thr’ Transducin, & phosphodiesterase, lowers CGMP, thus closing most f Na+ channel Transducin : Regulatory protein a. guanine nucleotide binding protein ( G- Protein)

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Night blindness: or Nictalopia One of the earliest signals of vit A deficiency Is impaiment of dark adaptation There should be continuous supply of retinol for nromal visual function. Vit A dept depress the resynthesisi of rhydopsin & interferes with the function of rods resulting in night blindness

DARK ADAPTATION: 

DARK ADAPTATION More photons are required to excite already illuminated rod, whereas only a few photons are sufficient to excite rod cell in the dark. This property is called Dark adaptation. TOTSTEN WIESEL was awarded Nobel Prize in 1981

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Bright light depletes stores of rhodopsin: When a person shifts suddenly from bright light to a dimly area there is difficulty to see. A few min,later,rhodopsin is resynthesised & vision is improved. This period is called Darkadaptation time.

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This is in vit A deficiency. Defi, of cis- retinal will lead to in darkadaptation time & night blindness.

Defeciency manifestation: 

Defeciency manifestation Night blindness: Visual acuity is diminished in dimlight Dark adaptation time is increased. 2. Xeropthalmia: Dry,thick,wrinkled, keranatised conjunctiva.

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3. Bitot spots: Greyish white triangular plaques firmly adherent to conjunctiva. (upto the reversible) 4. Keratomalacia: Xerophthalmia persisting for a long time progress to keratomalacia (softening of comes) degeneration of corneal epithelium & opacities develop.

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5. Preventable blindness: Most common cause of blindness in Indian children below the age of 5. About 40% preventable National blindness control programme give regular vitA supplementation to children L syn

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6. Skin & Mucous memb lesions Follicular hyperkeratosis / Phrynoclerma Respiratory tract infections Caliculi Acne. Others: Growth retardation due to defective syn of chondrotin so 4

HYPERVITAMINOSIS: 

HYPERVITAMINOSIS Alteration of skin & mucous memb. Hepatic dysfunction Headache, drowsiness, Peeling of skin about mouth discovered in Eskimos, after eating liver of polar bears.

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Causes of Vit A defi: Decreased in take Obstructive Jaundice Cirrhosis of liver- reduced syn of RBP Severe malnutrition Chronic nephrosis.

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Assessment of deficiency: Dark adaptation test: Increased in vit A deficiency 2. RBP – in serum decreased 3.Vit A in Serum decreased Colorimetric measurement based on Carr & Price reaction : Spectrophometry – absorption at 325nm.

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B.Caratene as Antioxidant: Help to trap free radicals in tissues prevents heart attacks. Retonic acid functions: Role in gene expression & Tissue differentiation Role in GP syn Role in Mps syn – essential for sulfation of MPS in matrix of cartilage & bones.

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4. Collagen breakdown: Retonic acid – enzyme collagenase & prevents breakdown of coll. 5. Role in Keratinisation : Prevents ‘K’ of epi keeps mucous memb healthy. Therapeutic uses: Uses in Oral leukoplasia, precancerous condi Promyelocytic leukamia.

DIETARY SOURCES: 

DIETARY SOURCES ANIMAL: Liver oil,buttermilk, cheese, egg yolk Plant : In the form of Provit carotene,Tomatoes,carrots,green-yellow vegetables,spinach,fruits such as mangoes,Papayas,Corn,Sweet Potatoes. Spirulina: (algae) – Good source of Vit A

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Abs: Vit A precursors are abs. in S.I in the presence of bile salts dietary vit A is in ester form. Hydrolyses by cholesterol esterase into F.A & free Vit A Free Retinol is abs & undergoes reesterification in intestinal epithelial cells. Liver is the only organ where carotena are converted to vit A Storage : stored in liver as retinylester ( retinyl palmitate)

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Transport: Retinol is transported with RBP 95% is stored as ester in itocells of liver released into plasma when required. - 10-20 mg of vit A present per 100 g of liver.

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Blood level : Vit A – 18 – 60 ug/dL Carotenaids - 100 – 300ug/dL D/R : Activity is expressed as I.U I.U = 0.3 ug of Retinol or = 0.341+ug of Retinyl ace tale or = 0.6 ug of β – Carotene also expressed as “Retinal equivalent”.

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1Retinalequivalent = 1 ug of Retinol Adult – (3000)IU/ day 5000 Functions: Role in vision Role in Reproduction – no conception takes place unable to carry pregnancy. Role in Epithelialisation Role in Bones& Teeth formation Role in growth.

SKIN & MUCOUS MEMB SHOWS GRAIS CHANGES: 

SKIN & MUCOUS MEMB SHOWS GRAIS CHANGES Skin : becomes dry,scaly,rough KERATINISATION Lacrimal glands: Dryness of conjuctiva & cornea- XEROPHTHALM Cornea: Whote opaque spots on conjuctiva BITOT SPOTS epithelium becomes keratinised Softened & ukerated “KERATOMALACIA”

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Resp tract: Keratinisation of mucous memb. Leads to infec & lowered resistance. Urinary tract : Keratinisation leads to calculi 4. Bone : Bone becomes cancellous, losing its structure, damages to brain & cord. Teeth : Thinning of enamel & chalky deposits.

VITAMIN - E : 

VITAMIN - E Isolated from wheat germ oil in 1936 Tocopherol Tokos = Child birth Pheros = to bear ol = alcohol Anti- infertility vitamin Most potent biological antioxidant

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Chemistry: Has a chromane ring with an Isoprenoid side chain – 8- Naturallu occuring Tocopherols. α - Tocopherol – 5,7,8, -trimethyl tocol β –Tocopherol- 5,8, dimethyl tocol r- Tocopherol – 7,8, dimethyl tocol Delta Tocopherol – 8 methyl tocol

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The presence of phenolic – OH group on 6 th carbon of the chromane ring is the most imp- group for its antioxidant activity