Vitamins are organic compounds that are needed by the human body in small amounts. They are not a source of energy but are essential for many functions including metabolism, vision, growth, and immune function. There are two types - water soluble vitamins that are not stored in the body and fat soluble vitamins like vitamin A that are stored. Vitamin A is important for vision, immune function, cell growth and reproduction. A deficiency can cause night blindness while too much can lead to toxicity issues like bone problems and liver damage. It is found in foods like liver, cheese, sweet potatoes and carrots.

1. Vitamins

2. Characteristics of Vitamins
 Needed in milligrams or micrograms
 Organic compounds, human body makes a few,
rest come from food
 Work with hormones
 Needed for the metabolism of other nutrients
 Are NOT cure-alls
 Do not supply energy; do not supply building
materials for the body
 B-vitamins are necessary to convert food to
energy; need based on calorie intake

3. Vitamins are organic, non-caloric nutrients essential
in small quantities for growth & good health
Water-Soluble
 Thiamin (B1)
 Riboflavin (B2)
 Niacin (B3)
 Vitamin B-6
 Folate (folacin, folate
acid)
 Vitamin B-12
 Pantothenic Acid
 Biotin
 Vitamin C (ascorbic
acid)
Fat-Soluble
 Vitamin A
 Vitamin D
 Vitamin E
 Vitamin K
A,D,E,K – “Australia Does
Export Kangaroos”

4. Important Features of Vitamins
1. Role in body
2. Food sources
3. Main deficiency symptoms
4. Main toxicity symptoms

5. Traits of water-soluble vs fat-soluble vitamins
Water-Soluble
 Dissolve in water (easily
lost in cooking)
 Are easily absorbed &
excreted if eaten in
excess
 Are not stored
extensively in body
tissues (Deficiency
develops in few weeks
or months)
 Seldom reach toxic
levels
Fat-Soluble
 Dissolve in lipid (with
exception of E are not
easily lost in cooking)
 Require bile for
absorption and
chylomicrons for
transport; enters
lymphatic before
entering blood
 Are stored in body
tissues liver and
(adipose); deficiency
takes longer to develop
 May be toxic in excess

6. Fat Soluble Vitamins - A
 2 forms – pre-formed Vitamin A (retinol, retinal
and retinoic acid ) and B-carotene (precursor) =
antioxidant as well as other carotinoids
 B-carotene is precursor, orange; chlorophyll masks
orange color in dark green leafy vegetables,
carotenoids are involved in photosynthesis
 Function = vision, eye health, formation of body
tissues, viability of reproduction, hormones, cancer
protection

7. Chemical Names
Vitamin A has three forms (all forms are called retinoids)
Retinal (the aldehyde form)
Retinol (the alcohol form)
Retinoic Acid (acid form or the active hormone)
Beta carotene – precursor or provitamin vitamin A
Retinyl acetate – used in vitamin supplements

8. Vitamin A: Structure and forms
Retinol-binding protein (RBP) transports retinol in blood. Deficiency of mineral
zinc interferes with Vitamin A metabolism by reducing retinol binding protein.
Retinol binding protein is complexed with the transporter of thyroxine to prevent
loss in kidneys.
The carotenoid with
most vitamin A
activity

10. Food Sources
 Retinol: Liver (richest source), fortified milk, whole milk,
cheese, cream, eggs, butter and fish liver oils
 Fortified Margarine
 Fortified Ready-to-Eat Cereals
 Beta-carotene: spinach and other dark leafy greens;
broccoli, deep orange fruits and vegetables (squash,
carrots, sweet potatoes, pumpkin)
 Nutritional supplements contain Vit. A as retinol, and/or
Beta-carotene in doses equaling or sometimes exceeding
the recommended dietary allowances (RDAs)
 Foods contain very little retinal or retinoic acid

11. Source of Vitamin A
Egg yolks are a good source of vitamin A (retinol).

12. Food Sources of Beta-Carotene
The carotenoids bring colors to meals; the retinoids allow us to see them.
Vitamin A in
foods
The colors of
vitamin A foods
Vitamin A- poor
are fast foods

13. Recommended Dietary
Allowances (RDAs)
 RDA for vitamin A is expressed in Retinol
Activity Equivalents (RAE)/day
 The measurement for vitamin A is in
micrograms (µg RE)
 Conversion factor: 1 International Unit (IU)
retinol=0.3 µg retinol equivalent or 6μg of β-
carotene
 Upper Level for adults: 3000 µg/day

14. Vitamin A Nutrient Intake
-Retinol activity equivalents
(RAE)
Age in years µg RE or RAE
Infants 0-8 400-500
Males 9-13 600
Males 14 and up 900

15. Vitamin A Nutrient Intake
Age in years µg RE or RAE
Females 9-13 600
Females 14 and up 700
Pregnant ≤ 18 750
Pregnant 19-50 770
Lactating ≤ 18 1200
Lactating 19-50 1300

16. Retinoids and carotenoids
Vitamin A activity
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17. Carotenoids-Conversion
 Beta carotene 15, 15'-dioxygenase converts beta
carotene into retinal. This reaction also requires
niacin
 In theory beta-carotene can produce 2 molecules of
retinal, but in vivo this does not occur because the
activity of beta-carotene 15, 15'-dioxygenase is very
low
 12 µg of beta-carotene= 1 RAE = 1 µg vitamin A
 24 µg of other carotenoids (alpha or gamma
carotene)= 1 RAE (retinol activity equivalents)
refers to correction factor for carotenoids

18. Carotenoids-Structures (1)

19. Metabolism of Vitamin A
(Digestion)
 Dietary vit A from animal sources is available in
form of retinyl esters. Pancreatic lipase hydrolyses
theses esters to releases retinol and fatty acids.
 Absorption requires bile acids and in the intestinal
cells retinol is esterified back secreted with the
chylomicrons.

20. Fate of the Carotenes
 Carotenoids are absorbed intact through
the intestinal wall.
 In the intestinal mucosa, β-carotene is then
cleaved by β-carotene15, 15‘-dioxygenase into
retinal (contains selenium)
 Retinaldehyde is reduced to retinol by
retinal reductase and esterified just like the
animal retinol and secreted into the
chylomicrons.

22. Metabolism of Vitamin A
(Transport to Liver)
 Chylomicrons deliver retinyl esters and
carotenoids to bone marrow, spleen, adipose
tissue, muscle, lungs and kidneys
 Chylomicrons remnants deliver retinyl esters
and some carotenoids not taken up by
peripheral tissue to liver
 When carotenoids reach the liver, a small
portion is cleaved to form retinol
 Some carotenoids are incorporated into HDL
(High density lipoprotein) or very low-density
lipoproteins (VLDLs) then become LDL (Low
density lipoprotein) and go into circulation

23. Metabolism of Vitamin A
(Storage in Liver )
 70-80% of body Vitamin A stores are in the
liver as retinol esters
 15% in adipocytes
 Remainder in kidney, ovary and intestine
 Some carotenoids can be stored in the liver,
unconverted carotenoids can be deposited in
fat tissue, leading to yellow color of animal fat

24. Functions of Vitamin A
 Vision
 Retinoic acid maintains cornea of the eye
 Epithelial cells, mucous membranes, skin
 Cellular Differentiation and Proliferation
 Retinoic acid and embryogenesis, particularly fetal
growth
 Growth, regulation of gene expression
 Reproduction
 Cell Surface Functions
 Bone Development (Bone remodeling), tooth growth
 Immune system function

25. Vitamin A – Deficiencies
Very common in children under five years old
especially in developing countries
 Ocular- night blindness (reversible) Xerophthalmia
(complete blindness)
 Impaired Immunity - Impaired immune function-decreased
T-cells more susceptible to infections
 Growth- abnormal body growth, anorexia, narrowing of
cranial cavity and spinal cord
 Dermatological- obstruction and enlargement of hair
follicles (plugging of hair follicles with keratin, forming
white lumps called hyperkaratosis), brittle hair as well as
rough, dry skin
 Nervous system-ataxia, increased cerebrospinal fluid
causing headaches

26. Vitamin A (con’t)
 Toxicity = hypervitaminosis A :
 RBC’s break down (nose bleeds), rashes, dry skin
 Nausea, vomiting, vertigo
 Bone - increased activity of osteoclasts that withdraw calcium
causing reduced bone density
 Liver damage
 Brain - elevated pressure in brain (headaches) mimicking brain
tumor, neurological symptoms, irritability
 Blurred vision
 Hair loss
 High vitamin A during pregnancy can cause brain damage,
cleft palate, and other birth defects
 High dietary levels of beta carotene (Hypercarotenemia) are
not toxic but can cause (yellow palms and yellow feet)
especially in infants

27. Hypercarotenemia
 A condition caused by an accumulation of
carotenoids in the adipose tissue, causing
the skin of palms and soles of feet to
appear yellow-orange

28. Deficiencies May Develop
 Individuals with fat malabsorption disorders-
steatorrhea, pancreatic, liver, or gallbladder
disease may develop deficiency. They may
need vitamin A supplement. Aquasol A,
water-miscible form of vitamin A, can be used
 Measles infection-depletes liver stores of
vitamin A often results in blindness
 Serious infections and parasitic infections
(worms in gut), constant bleeding and
diarrhea lead to malabsorption of fat and
vitamin A

29. 11-cis-retinal – binds to protein opsin to form rhodopsin,
which is needed for night vision and other light receptor
pigments. ( Retinoic acid will not work in visual cycle, do
Vitamin A and Vision
 One of the major
roles of vitamin A
is to aid in vision.

30. Vitamin A’s Role in Vision
As light enters the eye, pigments within the cells of the
retina absorb the light.

31. A derivative of vitamin A,
11-cis-retinal, participates
in the visual cycle under
low-light conditions. 11-cis-
retinal is coupled to the
protein opsin. Together
they form the photoreceptor
of the retinal rod cells of
eyes i.e rhodoposin. When
light falls on the retina, 11-
cis-retinal is isomerized to
all-trans-retinal leading to
conformational changes in
opsin with dissociation of
all-trans-retinal.

32. Vitamin A’s Role in Vision
Each pigment molecule (in this diagram, rhodopsin) contains11-cis retinal
(an active form of vitamin A) and a protein (in this diagram, opsin).

33. Vitamin A’s Role in Vision At the same time, a nerve
signal is sent to the brain.
All trans-retinal is
isomerized to 11-cis-
retinal by retinal
isomerase. The
regenerated 11-cis –retinal
reused in the visual cycle
to form rhodopsin. If
destroyed or damaged new
retinol must be obtained
from plasma. A deficiency
of vitamin A reduces the
light-sensitivity of the eye
leading to night blindness.

34. The visual cycle

35. Night Blindness
Normal vision person and vitamin A deficient
person sees headlights

36. Night Blindness
After car has passed, normal vision person
sees a wide stretch of the road

37. Night Blindness
The vitamin A deficient person can barely see a
few feet ahead and cannot see the road sign at all

38. Individuals suffering from night blindness not only see poorly at
night, but also require some time for their eyes to adjust from
brightly lit areas to dim ones. Contrast vision may also be
greatly reduced.
Normal vision Night blindness
Night Blindness

39. •Night blindness: A person can not see in the dim light
•Bitot´s spots: Triangular, foamy, soapy and gray or whitish
patches on the white part (the conjunctiva) of the eye.
•Conjunctiva xerosis: Dryness, roughness or wrinkles in the white
part of the eye. Changes of the tear ducts also lead to reduced wet
ability of the eye.
•Corneal xerosis: Surface of corneal is cloudy and dry.
•Keratomalacia : Softening of cornea, ulcers or holes may form.
Part of contents may come out.
•Xerophthalmia: Corneal scarring and blindness.
Progressive Development of Blindness

40. Whitish or gray triangular patches on white part of eye
are Bitot’s spots.
Photograph of Bitot’s Spots

41. Vitamin A deficiency-stages of eye
lesions to xerophthalmia
Conjunctiva
xerosis-
dryness or
wrinkles in
white part
Corneal xerosis
Dryness and
clouding of
corneal
Keratomalaci
a softening of
cornea, ulcers
or holes may
form
Xerophthalmia
Corneal
scarring and
blindness

42. Photograph of Xerophthalmia
Blindness due to vitamin A deficiency

43. Xerophthalmia results in blindness

44. Vitamin A deficiency affects sight in rat. This eye damage
may be far too advanced to be repairable by providing
vitamin A back into the diet.

45. Vitamin A deficiency is a world health problem. It is most common
in India, Africa, Latin America and the Carribbean. Caused by
Poor intakes of vitamin A, lack of; fat (to absorb); lack protein (to
transport), and lack of zinc (to mobilize from liver stores)

46. Follicular Hyperkeratosis
Skin lesions distinguishable from “goose
bumps” because they do not go away
when the skin is rubbed.

47. Vitamin A Deficiency and Toxicity
As the dose increases from zero, normalcy is reached. Intakes are
safe over a wide range, and then toxicity is reached.

48. People at risk for Vitamin A
deficiency
 Malnourished infants and young children
(males)
 People who are unable to absorb fat –
vitamin A needs to be co absorbed with
fat
 People with cirrhosis (other liver
diseases) –cannot store the vitamin

49. Signs of Vitamin A Toxicity
 Gingivitis
 Cheilosis
 Anorexia
 Irritability
 Fatigue
 Hepatomegaly
and abnormal
liver
function
 Ascites and portal
hypertension
 Serum vitamin A of
250-6600IU/100mL
 Bone pain and
fragility
 Hydrocephalus and
vomiting (infants
and children)
 Dry, fissured skin
 Brittle nails
 Hair loss (alopecia)
Copyright © 2000 by W. B. Saunders Company. All rights reserved.

50. Vitamin A Toxicity
Alopecia (hair loss)
from vitamin A toxicity
Shows recovery of
patient when vitamin A
supplementation
discontinued

51. Vitamin A Toxicity- Fissured
Fingernail
90,000 IU/day for 10 yrs.

52. Vitamin A Toxicity – Acne (7)
Face on the right after 3 months of treatment with
vitamin A acid (tretinoin) and benzoyl peroxide
Accutane is a very effective treatment for acne but can cause severe
birth defects. All women should be aware of this!!!

53.  Vitamin A toxicity
and birth defects
have been observed
among newborns
whose mothers used
Accutane (13 cis-
retinoic acid) also
known as Retin-A
cream
(tretinoin)during
pregnancy.

54. Vitamin A – Interactions with
Other Nutrients
Iron status-the microcytic anemia of
vitamin A deficiency can be corrected when
supplied with vitamin A
Vitamin A may affect iron metabolism or
storage or differentiation of red blood cell.

55. Vitamin A – Interactions with
Other Nutrients (cont.)
 Vitamin E-may inhibit beta-carotene
absorption or conversion to retinol in the
intestine
 Vitamin K-interfers with vitamin A absorption
 Zinc deficiency-needed for Retinal Binding
Protein synthesis so plasma retinol
concentrations decrease and liver
concentrations increase (night blindness can
occur from zinc deficiency)
 Alcohol dehydrogenase in peripheral tissue
converts retinol to retinal is dependent on zinc

56. Vitamin A – Interactions with
Other Nutrients (cont.) (3,5)
 Activity of retinyl ester hydrolase which releases
retinol from its ester storage form is zinc
dependent, Zn deficiency decreases hepatic
mobilization
 Alcoholism causes low zinc levels because of
inadequate dietary intake, decreased intestinal
absorption and increased urinary excretion.
 Zinc supplements of 600 mg/day can be given to
improve night blindness but caution is necessary
because it can cause copper deficiency
 Copper deficiency is common with zinc
supplementation

57. In Summary
 Other names
 Retinol
 Retinal
 Retinoic acid
 Precursors are carotenoids
such as beta-carotene
 2001 RDA
 Men: 900 g RAE/day
 Women: 700 g RAE/day
Copyright 2005 Wadsworth Group, a division of Thomson Learning

58. In Summary
 Upper level for adults: 3000
g/day
 Chief functions in the body
 Vision
 Maintenance of cornea,
epithelial cells, mucous
membranes, skin
 Bone and tooth growth
 Reproduction
 Immunity
Copyright 2005 Wadsworth Group, a division of Thomson Learning

59. In Summary
 Significant sources
 Retinol: fortified milk, cheese,
cream, butter, fortified
margarine, eggs, liver
 Beta-carotene: spinach and
other dark leafy greens;
broccoli, deep orange fruits
(apricots, cantaloupe) and
vegetables (squash, carrots,
sweet potatoes, pumpkin)
Copyright 2005 Wadsworth Group, a division of Thomson Learning

60. In Summary
 Deficiency disease:
hypovitaminosis A
 Deficiency symptoms
 Night blindness, corneal
drying (xerosis), triangular
gray spots on eye (Bitot’s
spots), softening of the cornea
(karatomalacia), and corneal
degeneration and blindness
(xerophthalmia)
Copyright 2005 Wadsworth Group, a division of Thomson Learning

61. In Summary
 Deficiency symptoms
(continued)
 Impaired immunity
(infections)
 Plugging of hair follicles with
keratin, forming white lumps
(hyperkaratosis)
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62. In Summary
 Toxicity disease:
hypervitaminosis A
 Chronic toxicity symptoms
 Increased activity of
osteoclasts causing reduced
bone density
 Liver abnormalities
 Birth defects
Copyright 2005 Wadsworth Group, a division of Thomson Learning

63. In Summary
 Acute toxicity symptoms
 Blurred vision
 Nausea, vomiting, vertigo
 Increase of pressure inside
skull, mimicking brain tumor
 Headaches
Copyright 2005 Wadsworth Group, a division of Thomson Learning