water soluble vit for class

8/8/2019 Water Soluble Vit for Class

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THE WATER-SOLUBLE VITAMINS

B-vitamins and vitamin C


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VITAMINS


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WATER SOLUBLE VITAMINS

Most are coenzymes, deficiencies result in

abnormal metabolism

Acute tox

icity unlikely due to

ability to

excrete

excesses

Microbial synthesis in ruminants or cecal

fermenters


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B VITAMINS

Originally thought to be one vitamin

Actually, there are eight (maybe more) of them

Act primarily as coenzymes in metabolicpathways

Important for ATP production!!!

Impo

rtant fo

rM

ANY additio

nal functio

ns


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B VITAMINS

Dietary requirement is linked closely to metabolic rate

(i.e., production)

Ruminant requirements met by rumen bacterial

synthesis

Hindgut bacterial synthesis and absorption is

insufficient to meet full requirements for a horse or

most colonic fermenters

Caprophagy helps recycle and better utilize vitamins for

cecal fermenters


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B VITAMINS - SOURCES

VARIETYof feedstuffs!

Plant sources Found in fibrous portion of

plants

Most cereals and grainproducts are enriched

Animal sources Liver

Milk

Egg

Beef, pork and chicken


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B VITAMIN - DEFICIENCY

LOTS of symptoms including fatigue

Specific diseases for each vitamin deficiency

(e.g., beriberi, pellagra)


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FACTORS AFFECTING

THIAMIN REQUIREMENTS Carbohydrate intake

Thiaminase intake

Raw fish

Bracken fern poisoning in ruminants and horses muscle tremor, incoordination, frequent falling, bradycardia and

cardiac irregularity

Excess sulfur in ruminant diets

(decreases thiamin synthesis)


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THIAMIN (B1) - DEFICIENCY

Polyneuritis retraction of head in chicks

In ruminants, polioencephalomalacia or stargazing (headretracted)

Cardiovascular disturbances

Beriberi heart enlargement, numbness

Bradycardia slow heart rate

Severe thiamin deficiency in alcohol abusers: Wernicke-Korsakoff syndrome

Diso

rientatio

n Loss of short term memory

Jerky eye movements

Staggering gait


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POLYNEURITIS (STARGAZING)


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Thiamin Deficiency - Polyneuritis

Thiamin-deficient rat shows typical arched

back and hyperextended hind legs

Same rat 8 hours after receiving thiamin

hydrochloride has normal use of its hind legs

and normal vestibular reaction


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RIBOFLAVIN (B2) - SOURCES

Milk and milk products

Enriched products

Liver


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RIBOFLAVIN

Absorbed by small intestine via active transport

Stable when heated

Breaks down in light and radiationMilk sold in opaque/translucent containers


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RIBOFLAVIN - DEFICIENCY

Reduced growth

Ectodermal lesions

Curled-toe paralysis in birds

Due to nerve degeneration

Cataracts (swine)

Moon blindness in horses

Joint stiffness in swine

Ariboflavinosis

Inflammation of the mouth, skin, eyes, and GI tract


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CURLED TOE PARALYSIS


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Riboflavin Deficiency

(A) Generalized dermatitis & growth failure

(B) After 1 month riboflavin treatment

(C) After 2 mo

nths treatment


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Induced Riboflavin Deficiency

Clinical signs include angular stomatitis, seborrheic

dermatitis and scaly scrotal skin lesions

Blood vessels invade cornea - itching, burning and grittiness


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NIACIN - SOURCES

Milk; eggs, meat, poultry, fish,

Whole grains and enriched products

All protein containing foods


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NIACIN - DEFICIENCY

Niacin in grain not available to monogastrics

Deficiency

Reduced growth and appetite Black tongue dog

Pellagra farm animals and humans in poor areasof the world

Fiery inflammation of tongue, mouth and upper esophagus

Diarrhea, dermatitis, dementia, and death (the 4 Ds)

Redneck disease in niacin-deficient areas of the US

Major components of diet were the 3 Ms meat (mostly porkfatback), molasses, and meal (corn meal)

Confusion, depression, poor memory


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Early Pellagra - Glossitis

Dental indentations resulting from edema - lip & tongue margins scarlet


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Advanced Pellagra

Dermatitis of elbows due to friction - beginning of desquamation in the center oflesion


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Pellagra - Casals Collar or Necklace

Photosensitive dermatitis outliningexposed area of neck & lesions on back

of hands - sunlight or heat from a stovecan induce this reaction

Same patient after nicotinamidetherapy


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PANTOTHENIC ACID

Food sources:

Organ meats

Whole grains

Legumes

Unstable in heat

Destroyed by food processing


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PANTOTHENIC ACID - FUNCTIONS

Essential for the synthesis of fatty acids and membrane

phospholipids, including sphingolipids

Essential for oxidation of fatty acids and amino acids

Essential for the synthesis of steroid hormones Essential for the synthesis of hemoglobin

CoA contributes an essential acetyl group during the synthesis

of the neurotransmitter acetylcholine and to several

glycoproteins and glycolipids


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PANTOTHENIC ACID - DEFICIENCY

Deficiency is rare; the burning feet

Goose stepping - swine

Cannot bend hock joint (nervous system degeneration)

Reduced growth, dermatitis, diarrhea


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Pantothenic acid deficiency - Chick

Dermatitis in chick onpantothenic acid deficient diet

Three weeks after calcium pantothenateadded to diet, skin lesions cured


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PYRIDOXINE (B6) - SOURCES

Meat, fish, poultry, liver

Non-citrus fruits

Legumes


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Spontaneous Seborrheic Dermatitis

Dermatitis around eyes, nose,mouth similar to that produced by

pyridoxine antagonist

Same patient after 3 weeks ofpyridoxine ointment therapy


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Pyridoxine Deficiency

Edema & denuding of ears, paws &

snout

After 3 weeks of pyridoxine

hydrochloride


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COBALAMIN - SOURCES

Animal sources: meat, fish, poultry, eggs, shellfish,

milk/products

Plant sources: none

Microbes!!


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VITAMIN B12, COBALAMIN

Not synthesized by plants

Animal-protein factor

Often deficient in monogastric diets

Microbes synthesize B12 Cobalt required

Some B12 synthesized in the hindgut

Not enough for most hind-gut fermenters, except horses


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COBALAMIN ABSORPTION

HCl and pepsin in the stomach release B12 from

protein foods

Requires intrinsic factor for absorption

Secreted by parietal cells Only essential function of stomach

Intrinsic factor attaches to B12 and the whole complex

passes to the small intestine where the gradual

absorption of B12 occurs


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COBALAMIN - DEFICIENCY

Deficiency often caused by inadequateabsorption rather than poor intake Lack of HCl or lack of intrinsic factor

Without HCl, the vitamin cannot be released from protein, andcannot attach to intrinsic factor

Atrophic gastritis: Common in geriatric animals - stomach cells get damaged

Could also be due to iron deficiency or Helicobacter pylori

No

healthy cells - decreased HCl and intrinsic facto

r Result is pernicious anemia due to a combination of atrophic

gastritis and lack of intrinsic factor

Other factors are defective gene for intrinsic factor, orif the stomach is injured or damaged


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COBALAMIN - DEFICIENCY

Reduced growth

Anemia

Pernicio

us anemia in humans (lack intrinsic facto

r)Macrocytic anemia (large red blood cells)

Neural symptoms

Wasting disease in ruminants (Co deficiency)


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COBALAMIN AND FOLATE

High dose of folate masks B12 deficiency

In both deficiency states, the first symptom is that the bloodcells grow rapidly

Either of the vitamins will be effective in resolving symptoms- however if folate is administered when B12 is needed, thesituation will be disastrous

Results in devastating neurological symptoms

B12 deficiency leads to nerve damage caused by destruction ofmyelin sheaths that protect the nerves

Note: folate can clear the blood symptoms but cannot stop the nervedamage


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PerniciousAnemia

Vitamin B12, FolicAcid,AscorbicAcid

Deficiency

Tongue pale & shiny; papillae atrophied inthe course of the glossitis which is often the

first symptom of the disease. The tonguemay become red and sore; these symptoms

usually subside promptly with appropriatenutritional therapy


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PerniciousAnemia Bone Marrow Smears

Smear showing megaloblasts,characteristic of certain anemias

Within 48-72 hours after treatmentwith vitamin B12, megaloblasts

replaced by normoblasts


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FOLATE - SOURCES

Animal sources

Liver

Crab meat

Plant sources Green forage crops

Legumes

Seeds

Unstable; destroyed by heat and oxygen Caution with feed processing, preparation and storage


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FOLATE (FOLIC ACID)

Involved in protein metabolism

Critical role in the synthesis ofDNA

Involved in new cell development

Requires the help of the vitamin B12

Folate is secreted into the GI tract with bile

If the cells of the GI tract are injured/destroyed as in the

case of alcohol abuse, then folate can not be absorbed, and

leads to deficiency


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FOLATE - DEFICIENCY

Macrocytic or megaloblastic anemia, and GI tractdeterioration Diarrhea, fatigue, depression and confusion

Impairs cell division and protein synthesis

Reduced growth Alters DNA metabolism

Folate deficiency masks vitamin B12 deficiency

Folate status affected by drugs with similar chemicalstructure Can lead to secondary deficiency

Many anti-cancer drugs can create deficiency of folate toothernormal cells

Antacids and aspirins interfere with folate

Smoking and oral contraceptives affect folate status


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Folate - Deficiency

Pregnant women prone to deficiency

Studies have documented the need for folate toreduce the risks of neural tube defects

Spina bifida in humans

Folate deficiency in early pregnancy, especially around 3 weeks afterconception


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FolicAcid Deficiency - Chick

Deficient chick is stunted, poorlyfeathered and severely anemic

Supplemented with 100 mg/kg folic acid -normal growth rate, feathering, and blood

values


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BIOTIN - SOURCES

Animal sources - organ meats, egg yolks, fish

Plant sources - soybeans, whole grains

Stable to

heat


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BIOTIN - DEFICIENCY

Avidin binds biotin

Found in raw egg white

Bond broken by heating to 100C

Deficiency sympt

oms

Cracked nails, hooves, dermatitis, hair loss

Dermatitis

Perosis

Fatty liver and kidney syndro

me, a fatal metabo

licdisorder in chicks and turkey poults


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Biotin Deficiency Rat

Generalized alopeciaSame rat 3 weeks after biotin wasadded to diet

Normal rat


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CHOLINE

Food sources;

Milk, liver, eggs and legumes

Synthesized in body

Methionine can be converted to choline

in liver


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CHOLINE - DEFICIENCY

Deficiency may cause liver damage

Fatty liver; kidney degeneration

Pero

sis chicks Slipped tendon

Malformation of leg bone


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Choline Deficiency - Human

Fatty infiltration of liver Treated with moderate fat diet pluscholine


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ASCORBATE - SOURCES

Vitamin C is also known asascorbic acid, ascorbate

Found in citrus fruits, cabbagetype of vegetables, greenleafy vegetables, cantaloupe,strawberries, lettuce,tomatoes, potatoes, papayaand mango

Destroyed by exposure tooxygen

Destroyed by heat


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VITAMIN C

Most mammals synthesize ascorbate from

glucose including farm animals

Primates and guinea pigs require a dietary source

of vitamin C


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VITAMIN C (ASCORBIC ACID)

Antioxidant Protects cells from free radicals

Protects iron from oxidative damage, thus enhancing ironabsorption in the gut

Assists as co-factor in collagen formation Collagen is the main structural protein in bones, teeth,

cartilage, tendons, ligaments, skin and blood vessels

Helps in the hydroxylation of carnitine

Conversion of tryptophan to neurotransmitters serotonin

and norepinephrine Enhances iron absorption and regulates the absorptionof copper


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OTHER POTENTIAL FUNCTIONS

Reduce stress (e.g., infections, smoking)

Mechanism unknown, but vitamin C requirements

increase during stress

Common cold? Disease prevention?

Cancer, heart disease: inconclusive


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VITAMIN C - DEFICIENCY

Scurvy in humans

Not in farm animals

Structural defects of bone, connective tissue

Bleeding gums; pinpoint hemorrhage

Fatigue; microcytic anemia

Loss of appetite

Slow wound healing; frequent infections

Scaly and dry skin; neurological symptoms

Edema

Loose teeth, gum problems

Diarrhea


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VITAMIN C - DISCOVERY

Prior to discovery, sailorson long-term voyagescommonly used to die

fro

m scurvy In 1930s James Lind

found that citrus fruits(limes used first)prevented scurvy byexperimentingon British

sailors Why Brits are called

limeys


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Vitamin C Scurvy in

Human Scorbutic Rosary

Enlarged costochondral junctions of

scurvy resembles rickets - lesions

may feel sharper & may be tender

X-ray of a child with scurvy


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Vitamin C Scurvy in Human

Gingivitis

Capillary fragility after application of a blood

pressure cuff


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ASCORBATE TOXICITY

Nausea, abdominal cramps and diarrhea

Interference with medical diagnostic tests

False positive or false negative to detect diabetes

Individuals taking anti-clotting medication maycounteract the effect if they take high doses ofvitamin C

Dangerous for people with iron overload


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REBOUND SCURVY

When high doses of vitamin C are taken, body

excretes it rapidly

When abruptly stopped, the body is unable to

immediately reduce rapid excretion rate

Potentially results in vitamin C deficiency


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water soluble vit for class

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