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Animal Nutrition > Vitamins and Minerals 3&4 > Flashcards

Vitamins and Minerals 3&4 Flashcards

1
Q

What do Vitamin E and Selenium partner as?

A

Antioxidants

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2
Q

What do we need antioxidants for?

A

Antioxidants scavenge free radicals

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3
Q

What are free radicals?

A

-are unstable molecules formed when an atom or molecule gains or loses an electron
-highly reactive

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4
Q

Where are free radicals produced?

A

-in cells during cellular metabolism

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5
Q

What can free radicals affect?

A

-lipids
-DNA
-proteins in cells

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6
Q

What do free radical produced by cells include?

A

-Superoxide’s: negatively charged oxygen molecule
-Hydrogen peroxide: not a free radical itself but can produce them

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7
Q

Who can antioxidants donate an electron to?

A

-a free radical to stabilize it

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8
Q

Will an antioxidant become unstable if it donates an electron to a free radical?

A

No

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9
Q

Is vitamin E fat or water soluble?

A

Fat soluble

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10
Q

What group of compounds is vitamin E apart of?

A

Tocopherols

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11
Q

What is alpha-tocopherol?

A

-Vitamin E
-the most biologically active of the tocopherols

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12
Q

Can other tocopherols have vitamin E antioxidant activity?

A

Yes

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13
Q

What are the functions of Vitamin E?

A

-important as a biological antioxidant
-helps prevent formation of peroxides

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14
Q

What can an antioxidant reduce?

A

-susceptibility of polyunsaturated fatty acid oxidative degradation

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15
Q

where are polyunsaturated fatty acids founds?

A

-cell membranes
-organelle membranes

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16
Q

What are peroxides?

A

-are toxic byproducts of incomplete polyunsaturated fatty acid oxidation

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17
Q

What is an example of a lipophile?

A

Vitamin E

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18
Q

Since vitamin E is a lipophile what can it be incorporated to? what else is there?

A

-membranes
-polyunsaturated fatty acids are found in the phospholipids of cell membranes

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19
Q

What are polyunsaturated fats open to attack from? and why?

A

-free radical
-bc of double binds in the polyunsaturated fatty acid

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20
Q

Symptoms of Vitamin E Deficiency

A

-reproductive failure
-myopathies
-nutritional muscular dystrophy
muscular weakness
-stiff gait
-white muscle disease

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21
Q

When there is a vitamin E deficiency that causes reproductive failure what happens?

A

-embryonic degeneration
-some effects in testicles of some species

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22
Q

When there is a vitamin E deficiency that causes nutritional muscular dystrophy what happens?

A

-muscle defects
-young animals will show stiff gait and weakness

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23
Q

When there is a vitamin E deficiency that causes white muscle disease what happens?

A

-dystrophic lesions in muscle
-white lesions on muscle show degeneration of skeletal muscle fiber
-degrading in cell membrane

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24
Q

What age group is white muscle disease most common in?

A

Young and growing animals

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25
Q

Supply and sources of Vitamin E

A

-Forages (whole plant feeds)
-Cereal grains
-Corn
-milk in mammal

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26
Q

What does corn contain more of?

A

-more relatively inactive forms of tocopherols

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27
Q

What do moist grains and hay experience during storage?

A

-loss of Vitamin E
-reduces avability

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28
Q

Do vitamin E requirements increase or decrease with greater polyunsaturated fatty acids in the diet?

A

-increase
-protection of feed quality as well

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29
Q

When and were was Selenium toxicity first observed?

A

-In grazing ruminants and horses in the west where high selenium soils caused disease (blind staggers or alkali disease)
-Many areas of US have Se deficient in soil

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30
Q

Can Selenium supplements reduce symptoms of Vitamin E deficiency?

A

Yes, but can’t fully replace or balance out deficincy

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31
Q

What is Seleniums Functions?

A

-Selenium is an essential component of the enzyme glutathione peroxidase (GP)
-contains selenocysteine amino acid in the active site of GP
-enzyme destroys hydrogen peroxide protecting cell membranes form peroxidative damage

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32
Q

Symptoms of Selenium Deficiency

A

-Muscular weakness
-muscle lesions in young ruminants
-very similar to Vitamin D deficiency

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33
Q

Sources of Selenium

A

-supplemented by injection
-oral dosing
-incorporation into salt blocks
~in Se deficient areas

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34
Q

Is there a large or narrow margin for Selenium?

A

-narrow margin of safety between the minimum requirement and the maximum requirement tolerable level
-supplement must be managed to avoid excess

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35
Q

What would a Se excess affect?

A

-liver and kidney damage
-hair loss
-hoof loss

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36
Q

What vitamin do all animals require a source of?

A

Vitamin A

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37
Q

Does active vitamin A occur in plants?

A

-No

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38
Q

What can be converted to get Vitamin A?

A

-Carotenoids from plants, like beta-carotene, can be converted to vitamin A

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39
Q

Characteristics of vitamin A deficiency and excess

A

-vitamin A deficiency is a widespread problem in animals and humans
-Vitamin A deficiency and excess are both serious hazards
-deficiency leads to disease

40
Q

What is provitamin A?

A

-Carotenoids
-not active form
-most abundant and widespread provitamin A in animal feeds is beta-carotene

41
Q

What is the active form of vitamin A?

A

-Retinol
-retinol includes a hydroxyl that allows it to be esterifies to a fatty acid

42
Q

What is the structure of vitamin A?

A

-All trans form: geometric orientation of the double bonds
-The hydroxyl (OH) group at the end is the side where fatty acids can be added using an ester bond
-half of beta carotene

43
Q

What is the structure of retinoic acid?

A

-Presence of carboxylic acid (OOH) group at the end where the hydroxyl (OH) group is on retinol

44
Q

How is vitamin A metabolized?

A

-Vitamin A and provitamin A carotenoids are absorbed with lipids from the small intestine
-Vitamin A is esterified (retinyl esters) for transport in chylomicrons into the lymph and bloodstream

45
Q

Where does most of the conversion of beta-carotene to vitamin A occur?

A

-intestinal mucosa

46
Q

Simple characteristics of vitamin A metabolism

A

-incorporated into mix micelles
-go to enterocytes (absorbed here)
-Into the lymph
-chylomicrons export into circulation

47
Q

How is vitamin A stored?

A

-about 90% of the body’s vitamin A is stored in the liver mainly in ester form
-carotenoids that escape conversion to vitamin A can be stored in tissues

48
Q

Why is Vitamin A storage important?

A

-for periods of dietary shortage
-deficiency might not produce symptoms for months bc of storage

49
Q

What happens to carotenoids (pigments including beta-carotene) that escape conversion to vitamin A

A

-Fat soluble vitamin so adipose tissue is one location
-humans, horses, cattle can all have yellow pigmented fat depending on carotenoid intake

50
Q

Where is a lot of carotenoids stored? and how?

A

-liver
-in ester form
-vitamin A droplets

51
Q

When will retinol be mobilized?

A

-low dietary intake

52
Q

What are the functions of Vitamin A?

A

-Vision
-cell growth and differentiation
-Retinoic acid

53
Q

What is vitamin A an essential precursor for? and what is it?

A

-the formation of rhodopsin
-rhodopsin is a visual pigment in the retina of the eye

54
Q

What is the primary event in visual excitation of the retina is the isomerization?

A

-the isomerization of cis isomer leading to conformational changes in rhodopsin
-hyperpolarization of the retinal rod cell
-extremely rapid transmission of electrical activity to the brain via the optic nerve

55
Q

Why is Vitamin A important for vision?

A

-trans-retinal is isomerized to cis-retinal in the dark, which associates with opsin to regenerate rhodopsin

56
Q

Why is vitamin A important to cell growth and differentiation?

A

-through the acid form of vitamin A you get retinoic acid

57
Q

How is retinoic acid formed? and what does it interact with?

A

-formed in cells from retinol taken up from the blood
-interacts with a cellular protein receptor to turn on (or off) genes in the nucleus of cells
~including skin and gut cells, bone, ovary, testis
~especially important for embryonic cell differentiation

58
Q

Whay are symptoms of Vitamin A deficiency?

A

-Night blindness: diminished ability to see in dim light
-Epithelial tissue defects
~diarrhea: gut
~kidney and bladder stones: urinary system
~rough, hairy, scaly skin
-Anormal bone development of fetus and neonates

59
Q

What are sources of vitamin A fat soluble?

A

-fish oils, milk fat, egg yolk are good sources from animals
-as long as animals producing them were not vitamin deficient

60
Q

What are sources of provitamin A carotenoids?

A

-green forages are good sources for grazing livestock
-grains have little beta-carotene
-yellow corn has ahigh proportion of non-beta-carotenoids with less vitamin A value than beta-carotene

61
Q

What happens to carotene content of forages with maturity and storage?

A

-carotene content of forages declines with maturity and declines with storage for hays and silage

62
Q

Symptoms of Vitamin A toxicity?

A

-high levels of Vitamin A can cause skeletal malformation, spontaneous fractures, internal hemorrhage, and other symptoms

63
Q

What are the safe levels of Vitamin A?

A

-upper safe levels are 4-10 times requirements in nonruminants
-30 times requirements in ruminants

64
Q

What can in influenced by other minerlas?

A

-availability, absorption, and sometime post-absorption utilization of essential minerals

65
Q

Well know mineral-mineral interaction?

A

-Na and K
-Ca and P
-Cu, Mo, and S (ruminants)

66
Q

What type of minerals are Cu, Mo and S?

A

-S (sulfur) is a macro mineral
-Mo (molybdenum) and Cu (copper) are trace minerals

67
Q

What is the most common imbalance?

A

-Induced copper deficiency from relatively high Mo and/or S levels
-induced copper with low Mo and or S levels

68
Q

What is the site of actions for the Cu-Mo-S mechanism interaction?

A

-rumen

69
Q

What can high levels of S or Mo cause?

A

-inhibits absorption
-high levels of both severely limits availability

70
Q

What does the Cu-Mo-S interaction cause?

A

-involves formation of insoluble Cu salts in the rumen
-sulfides and thiomolybdates (sulfides and molybdate salts combination)
-poorly absorbed

71
Q

What do B vitamins do?

A

-support enzyme reactions
-each has a distinct specific role

72
Q

What does oxidative decarboxylation require?

A

Coenzymes from
-thiamin (B1)
-riboflavin (B2)
-nicotinamide (niacin)
-pantothenic acid

73
Q

What does oxidative decarboxylation involve? What does it join?

A

-removal of a carboxyl (COO-) group from an organic acid
-joins the rest of the molecule with coenzyme A, forms CO2, and hydrogenated NADH

74
Q

What is Pantothenic Acid? What does it do?

A

-peptide of a butyric acid derivative and beta-alanine
-readily absorbed and circulates in blood plasma as the free acid

75
Q

What is Coenzyme A?

A

Pantothenic acid is a component of coenzymes A

76
Q

What enzymatic reactions utilize coenzymes A?

A

-pyruvate dehydrogenase
-propionate CoA carboxylase
-fatty acid synthetase

77
Q

Symptoms of Pantothenate Deficiency

A

-Reduce growth rate
-Dermatitis in chicks
-Fatty acid infiltration of the liver; fatty acids acclimate in liver
-Nervous system problems in pigs

78
Q

What happens to the nervous system in pigs with a pantothenate deficiency?

A

-peculiar gait: goose steeping
-results from nerve degeneration

79
Q

What is Niacin/Nicotinic Acid/Nicotinamide? What is it produced by?

A

-pyridine 3-carboxylic acid
-Niacin can be produced from tryptophan (essential amino acids) if available in excess of protein synthesis requirements
~limited efficiency: 60 units of tryptophan to produce 1 unit of niacin in pigs

80
Q

What are the two coenzymes of Niacin?

A

-NAD: nicotinamide adenine dinucleotide
-NADP: nicotinamide adenine dinucleotide phosphate

81
Q

What is Niacin and its coenzymes (NAD and NADP) important for?

A

-the transfer of hydrogen from substrates to oxygen: producing water
-lots of substrates are dehydrogenated by enzymes using these coenzymes to reduce the hydrogen ions
~receive H in dehydrogenated

82
Q

Symptoms of Niacin Deficiency?

A

-reduce growth
-reduce appetite
-diarrhea
-vomitting
-dermatitis

83
Q

Niacin Deficiency in specific animals

A

-ulcerated intestine are manifestation in pigs
-poultry can have poor feathering
-Dogs can get mouth lesions and darkening of tongue

84
Q

Where can Niacin be found?

A

-in grains, but can be bond and unavailable for absorption in non-ruminants

85
Q

What is Thiamin (B1)?

A

-Thiamin is phosphorylation in the liver to form thiamin pyrophosphate (TPP)
-TPP is an essential cofactor for decarboxylation enzymes including pyruvate dehydrogenase

86
Q

Symptoms of Thiamin Deficiency?

A

-disrupts carbohydrate and lipid metabolism
-decarboxylation is reduced and acetyl-CoA doesn’t enter the cycle (polyneuritis)
-Bradycardia (slow heart rate)

87
Q

What is a key metabolic for the citric cycle?

A

Pyruvate

88
Q

What is polyneuritis?

A

-a classical sign in chicks
-retraction of the head and ridigity of the legs
-Also reduced growth

89
Q

What id Riboflavin (B2)?

A

-ribose + isoalloxazine
-precursor required for flavin adenine dinucleotide (FAD) and flavin mono nucleotide (FMN)

90
Q

What is FAD responsible for?

A

-transferring H to NAD during pyruvate decarboxylation reaction
-FADH recycled (returns) to FAD so it is not shown in reaction

91
Q

FAD and FMN Synthesis Reactions

A

-riboflavin + ATP -> (flavokinase) FMN + ADP
-FMN + ATP -> (FAD pyrophosphorylase) FAD + pyrophosphate

92
Q

Symptoms of Riboflavin Deficiency

A

-reduced growth is apparent
-Poultry have curled-toe paralysis with deficiency: results from degeneration of myelin sheaths on nerves
-Lesions of the mouth, anorexia, loss of hair, stillbirth of piglets

93
Q

B Vitamins in Ruminants

A

-Microbes in the rumen produce B vitamins to support their own metabolism
-For Adult ruminants, microbes exiting the rumen and entering the small intestine provide sufficient B vitamins to meet requirements

94
Q

Is B vitamin supplementation necessary in ruminant young animal?

A

-Not really, B vitamin come from rumen, but in young animals most come from milk from mom
-If calf on formula, then yes supplement

95
Q

Is B vitamin supplementation necessary in non-ruminants?

A

-Yes, supply vitamin B to baby pigs bc have no rumen, but should be getting vitamin B from milk from mom

Animal Nutrition (22 decks)

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