Vitamins

Important
Questions and
Answers.
1) Describe the sources, RDA, functions, deficiency
manifestation, toxicity of Vitamin A (10 marks).
 Sources:
• Animal sources include milk, butter, cream, cheese, egg yolk and liver. Fish
liver oils (cod liver oil and shark liver oil) are very rich sources.
• Vegetable sources contain the yellow pigment β–carotene.
• Carrot contains significant quantity of β–carotene.
• Papaya, mango, pumpkins and green leafy vegetables (spinach, amaranth)
are other good sources.

 RDA: Recommended dietary allowance

• Adult woman = 750 µg/day.
• Adult men = 750 – 1000 µg/day.
• Children = 400 – 600 µg/day.
 Functions:
Retinal, retinol and retinoic acid have special biological functions.

1. Retinal for vision:

• Retinal form of vitamin A is required for vision. Rod cells and cone cells
present in retina are responsible for vision.
• Rhodopsin present in rod cells is responsible for vision in dim light and
photopsin present in cone cells is required for vision in bright light and
colour vision.
• Both these visual pigments contain vitamin A in the form of 11-cis retinal.

2. Normal reproduction:
Retinol plays an important role in normal reproduction.
3. Iron transport:
Retinol promotes the synthesis of transferrin (iron transfer protein) and
thus helps in iron transport, and hence Hemoglobin synthesis.

4. Normal epidermal growth:

Retinoic acid is essential for normal differentiation and mucous
secretion of epithelial tissue and it also prevents keratinization of
epithelial tissue.

5. Growth:
Retinoic acid is also required for growth, especially skeletal growth.

6. anti- carcinogenic effect. It functions as antioxidant and reduce the

risk of cancers caused by free radicals.
Deficiency:
Causes:
• Inadequate intake.
• Impaired absorption.
• Impaired storage.
• Impaired transport.
• Increase excretion of vitamin.

1. Night blindness or nyctalopia: Vitamin A is required for the vision in dim light
so deficiency of vitamin A causes night blindness.

2. Xeropthalmia (dryness of eye): Keratinisation occurs in cornea and conjunctiva

of eye causing dryness of these tissue.

3. Keratomalacia : If untreated Xeropthalmia results in corneal ulceration and

degeneration, a condition called as Keratomalacia, leading to total blindness.
4. Renal failure: Keratinization occurs in renal causing renal failure.

5. Respiratory infections: Keratinization occurs in respiratory tract.

With reduced mucous formation, there is atrophy of respiratory
epithelium, increasing the susceptibility to respiratory infections.

6. Reproductive failure.

7. Growth retardation.

8. Microcytic anemia, because vitamin is required for iron transport

and hence required for Hemoglobin synthesis.
 Toxicity:
• Excess consumption of vitamin A leads to the toxicity condition called
vitamin A toxicity or hypervitaminosis A. however, excess of beta
carotene is not toxic.
Causes:
• Accidental over ingestion as seen in hunters.
• Excessive intake by children because of overenthusiastic mothers.
• Inappropriate therapy for treating vitamin A deficiency.

Symptoms:
• pseudotumor cerebri.
• Head ache.
• Vomiting.
• blurring of vision.
2. Describe the sources, RDA, functions, deficiency manifestation,
toxicity of Vitamin D (10 marks).

 SOURCES:
Rich sources of vitamin D3 are:
• Fish liver oils such as cod liver oil, and shark liver oil.
• Egg yolk.
• Animal liver.
• Milk and dairy products such as butter.
Vitamin D2 present significant amount in molds and yeast.
 RDA:

• Children:10 µg/day.
• Adults : 05 µg/day.
• Pregnant women: 10 µg/day.
• Lactating women: 10 µg/day.

 Functions:

• The sites of action are:

1.Intestinal villi cells.
2.Bone osteoblasts.
3.Kidney distal tubular cells.
1.Vitamin D and Absorption of Calcium:

Calcitriol promotes the absorption of calcium and phosphorus from the intestine.

Calcitriol acts like a steroid hormone.

It enters the target cell and binds to a cytoplasmic receptor.

The hormone-receptor complex interacts with DNA and causes derepression and
consequent transcription of specific genes that code for calbindin.

Due to the increased availability of calcium binding protein, the absorption of

calcium is increased.
Calcitriol increases calcium absorption
2.Effect of vitamin D in bone:

Mineralization of the bone is increased by increasing the

activity of osteoblasts.

Calcitriol coordinates the remodeling action of osteoclasts and

osteoblasts.

 Calcitriol stimulates osteoblasts which secrete alkaline phosphatase.

Due to this enzyme, the local concentration of phosphate is increased.

The ionic product of calcium and phosphorus increases, leading to

mineralization.
3.Effect of vitamin D in Renal tubules:

Calcitriol increases the reabsorption of calcium and

phosphorus by renal tubules, therefore both minerals
are conserved (PTH conserves only calcium).
 Calcitriol

Direct action
induces the production Acts on osteoblasts which Increase
of calbindins which activates osteoclasts to calcium and
allow Ca2+ to be reabsorb Ca++ from the phosphorous
absorbed against a bone matrix. reabsorption.
high Ca2+ gradient In children helps in bone
remodelling
Causes for vitamin D deficiency:

Deficiency of vitamin D can occur in people who are not exposed to

sunlight properly, e.g. inhabitants of northern latitudes, in winter months, in
people who are bedridden for long periods, or those who cover the whole
body.
Nutritional deficiency of calcium or phosphate may also produce similar
clinical picture.
Malabsorption of vitamin (obstructive jaundice and steatorrhea). High
phytate content in diet may also reduce the absorption of vitamin.
Abnormality of vitamin D activation. Liver and renal diseases may retard
hydroxylation reactions.
Deficient renal absorption of phosphates.
Deficiency of vitamin D:
Vitamin D deficiency causes Rickets in children and osteomalacia in adults.
Rickets:
Rickets is a disease of growing bone. There is insufficient mineralization of
new bones. Bones become soft and pliable (easily bent). Rickets is
characterised by,
• Bowlegs.
• Knock knees.
• Pigeon-chest.
• Rickety-rosary (beaded appearance) of ribs.
Note: Renal rickets is seen in patient with chronic renal failure. Kidney is
required for the formation of calcitriol that is required for calcium
absorption and bone mineralization. So, chronic renal disorders lead to poor
bone mineralization and rickets, but respond to provision of calcitriol.
Osteomalacia:
Osteomalacia is caused due to the deficiency of vitamin D in adults.

Symptoms:
• Insufficient mineralization of bones.
• Softness of bones.
• Bone pain and aches.
• Easy fracture of bones.
Toxicity (hypervitaminosis):
Excess consumption of vitamin D leads to a toxicity condition –
hypervitaminosis D.

Symptoms:
• Demineralization of bones, hypercalcemia are main findings.
Calcification of soft tissues, especially renal tissues leading to renal
stones is one of the main features.
• Loss of weight, weakness, polyurea, increased thirst are the other
symptoms.
3. Explain walds visual cycle or dark adaptation mechanism or role
of retinal in vision in dim light.

• Rod cells of retina are responsible for vision in dim light. They contain
the visual pigment called rhodopsin (11-cis retinal + opsin).
• When the light falls on retina, a series of biochemical changes takes
place and rhodopsin is converted to meta rhodopsin (all –trans retinal
+ opsin), which is unstable.
• Subsequently, all-trans-retinal dissociated from opsin. This triggers a
nerve impulse, which is carried to the brain through optic nerve. (this
is the mechanism of vision in dim light).
• Role of retinal in vision in dim light:
Wald’s visual cycle:

• Now all-trans-retinal has to be converted back to 11-cis-retinal. This

process of regeneration of 11-cis-retinal is called Wald’s visual cycle
or Rhodopsin cycle or vitamin A cycle.
• First, all-trans-retinal is converted to all-trans-retinol by retinal
reductase (in the retina).
• All-trans-retinol is then transported to the liver.
• In the liver cells all trans-retinol is isomerized to 11-cis-retinol by the
enzyme isomerase.
• Then 11-cis-retinol is transported back to retina.
• In the retina, 11-cis-retinol is converted to 11-cis-retinal by the retinal
reductase enzyme. Now 11-cis-retinal can bind with opsin to form
rhodopsin.
Name Coenzyme form RDA Main reaction using the Deficiency
coenzyme disease

Thiamine Thiamine pyrophosphate 1–1.5 mg Oxidative decarboxylation of Beriberi

(TPP) alpha
keto acids

Riboflavin Flavin adenine 1.5 mg Dehydrogenation, oxidised in Glossitis, angular

dinucleotide ETC stomatitis
(FAD) (1.5 ATP)

Niacin NAD and NADP 20 mg Dehydrogenation, oxidised in Pellagra

ETC (2.5 ATP)

Pyridoxine Pyridoxal phosphate 1–2 mg Transamination, Seizures,

(PLP) decarboxylation of homocystinuria
amino acids
Name Coenzyme form RDA Main reaction using the coenzyme Deficiency disease

Pantothenic Coenzyme A, ACP 10 mg CoA derivatives, acyl carrier Burning foot

acid proteins syndrome

Biotin Biotin 30–40 Carboxylation No specific disease

microg
Folic acid Tetrahydrofolic acid 200 microg One-carbon group carrier Macrocytic anemia
(THFA)

Vitamin B12 Adenosyl B12, 1–2 microg Isomerisation of methyl malonyl- Megaloblastic
methylcobalamin CoA, anemia, Sub-acute
demethylation of homocysteine to combined
met degeneration

Ascorbic acid No specific form 75 mg Antioxidant property Scurvy