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Lecture

BPK 110 Lecture Notes - Vitamin A Deficiency, Retinoid, Xerophthalmia


Department
Biomedical Physio & Kines
Course Code
BPK 110
Professor
Gina Whitaker

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Kin110 Chapter 7 Vitamins (Fat Soluble)
Vitamin A
Vitamin A is found in two forms
Retinoids
-derived from animal sources
-preformed vitamin A (biologically active form)
-includes retinal, retinol, and retinoic acid
Carotenoids
-derived from plant sources (yellow-orange pigments)
-pro-vitamin form, converted to retinoid form by body as needed
Examples include β-carotene, lycopene, lutein
Functions
Vision
Retinal forms part of the molecule called rhodopsin
-rhodopsin is found in the cells of the retina (back of eye)
-important for converting a light stimulus to an electrical signal which allows brain to interpret
visual info
After entering the eye, light strikes the visual pigment rhodopsin, which is formed by combining
retinal with the protein pepsin
Light causes the retinal molecule to change from a bent to a straight configuration
A nerve signal is sent to the brain, telling that there is light, and retinal is released from opsin
Some retinal is lost in the cycle
Some retinal returns to its original configuration and binds to opsin to being the cycle again
When vitamin A status is normal, vitamin A from the blood replaces any retinal lost from the
cycle
When vitamin A is deficient, not enough vitamin A is available in the blood, and the
regeneration of rhodopsin is delayed. Until rhodopsin reformed, light cannot be perceived
Cell differentiation (immature stem cells specialized mature cells)
Vitamin A increases/decreases gene expression (the events of protein synthesis in which the
information coded in a gene is used to synthesize a protein)
E.g. express a specific gene which tells cell to make a specific protein which affects function of a
cell
Vitamin A promotes differentiation of epithelial cells
-skin, lining of eyes, intestines, lungs, vaginal tissue, bladder
Vitamin A promotes differentiation of T-lymphocytes
-immune function
Reproduction & Growth (due to its function in cell differentiation)
Retinol important for sperm development
Required for normal fetal growth
Important for bone remodeling (process by which old bone is removed and new bone is
formed) and growth
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Antioxidant (carotenoids only)
Donates an electron to oxygen free radicals to prevent them from stealing electrons from other
molecules
RDA = 700 ug (women) & 900 ug (men)
E.g. 100% RDA-1 cup sweet potatoes, ½ cup pumpkin, or ½ cup carrots
Deficiency
One of the most common nutrient deficiencies worldwide
Leading cause of preventable blindness
Deficiency due to lack of intake required 1-2 years to develop in adults (more quickly in
children)
-can also be due to a lack of fat intake
First detectable sign is night blindness (difficulty seeing in dim light which is reversible with
additional vitamin A)
-early stage of xerophthalmia (spectrum of eye conditions resulting from vitamin A deficiency
that may lead to blindness)
Increased incidence of infectious disease
Keratinization/Hyperkeratosis
-epithelial cells don’t differentiate properly and begin to secrete keratin instead of mucus
-keratin is a hard inflexible protein (found in hair and finger nails)
-later stage xerophthalmia is total blindness due to drying and hardening of the cornea
-skin becomes dry, rough and scaly
Toxicity
Only the retinoid form is toxic
Overconsumption of carotenoids is not harmful because conversion to retinoids is regulated in
the body however; it may lead to a harmless condition known as hypercarotenemia (a condition
caused by the accumulation of carotenoids in the adipose tissue, causing the skin to appear
yellow-orange)
Symptoms of Toxicity
-nausea, vomiting, diarrhea
-loss of appetite, fatigue, insomnia
-headaches, blurred vision, dizziness
-liver damage, bone fractures
-abnormal fetal development & birth defects
Vitamin A toxicity can be fatal
Vitamin D (The sunshine vitamin)
Can be obtained from the diet or the sun
-diet form is the inactive form
-vitamin D precursor made from cholesterol sits beneath the skin and is converted to inactive
Vitamin D by UV rays
Inactive Vitamin D is modified by both liver and kidneys to become active
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