antioxidants Flashcards

1
Q

we eat vitamin C in the form of _______________, which is a ___________, donating both _______s and _______s

A

ascorbic acid–> reducing agent that donates both e-s and Hs

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2
Q

when ascorbic acid donates an electron, what does it briefly become?

A

a free radical!

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3
Q

what two steps must occur for ascorbyl radical to be reduced back to ascorbic acid?

A

must donate another e- to become dehydroascorbic acid and then must be reduced back by glutathione

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4
Q

what does dehydroascorbate reductase need for structural purposes to reduce dehydroascorbic acid back to ascorbic acid?

A

selenium~

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5
Q

t/f: Vit C recycling is efficient

A

false! we need to have a constant dietary supply …

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6
Q

what is the deficiency of Vit C + symptoms?

A

scurvy: bruising, bleeding gums, CT issues, fatigue

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7
Q

what are the top 4 dietary sources of Vit C?

A

citrus, papaya, bell peps, brussels

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8
Q

what is the RDA for vit C?

A

m: 90 mg/d
f: 75 mg/d

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9
Q

how is ascorbic acid digested?

A

trick question! it’s not digested… we eat and absorb straight ascorbic acid

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10
Q

how is ascorbic acid absorbed(2 ways)?

A

diffusion(small molecule) and transporter

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11
Q

what is the % absorption of Vit C? how is this affected by high ingestion?

A

75-90%, but this drops with megadoses

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12
Q

how is ascorbic acid transported in the blood? how does it get into cells?

A

transported freely in the blood(very water soluble/polar)

needs transported to enter cells

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13
Q

t/f: high doses of Vit C are beneficial to increase serum levels in times of illness

A

false- at about 150 mg/dL, your blood is pretty much saturated and 1K+ mg/d is pretty useless..

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14
Q

at about 100 mg dosage of Vit C, what “storage” cells are saturated with it?

A

WBC: monocytes, lymphocytes, neutrophils

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15
Q

what is the theory of harm of taking Vit C at very high levels? what are 2 side effects of this?

A

can it act as a PROoxidant??? causing liver damage OR acting as a cancer killer?

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16
Q

____________ and ____________ are enzymes that insert O/O2 to a molecule

A

mono and dioxygenases

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17
Q

vit C acts as an e- donor to _______________(# and adjective) enzymes. how many mono and deoxygenases are each of those?

A

8 mammalian: 2 mono, 6 di

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18
Q

what are the 2 main monooxygenase functions of vit c?

A
  1. neurotransmitter synthesis: norepinephrine, serotonin

2. peptide hormone post translational modification

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19
Q

what 3 syntheses by deoxygenases does Vit C participate in?

A

collagen, carnitine, tyrosine(non essential AA)

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20
Q

what is the main function of carnitine in cells?

A

transports FA across mitochondrial membrane to undergo B oxidation in there

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21
Q

how many steps of collagen synthesis is Vit C a part of?

A

only 1!

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22
Q

after collagen gene is translated and transcribed what is formed? what must happen after this for collagen to be formed?

A

pre collagen peptide chain –> must undergo post translational modification

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23
Q

what process in post translation modification of the alpha collagen chain requires the Vit C dependent enzyme? why is Vit C needed, specifically?

A

hydroxylation–> Vit C needed to add OH to proline on the pre collagen chain and enzyme needs e- to be donated from Vit C to do this

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24
Q

during the post translation modification of the collagen, what happens to the deoxygenase AND Vit C?

A

both become oxidized… must be reduced back to donate e- and OH again

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25
Q

t/f: collagen synthesis will still occur with a vit C deficiency

A

true! but not as much…. deoxygenase will use any e- donor but Vit C is most efficient

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26
Q

after hydroxylation and sometimes ________________, the collagen chain is _____________ed extracellularly

A

glycosylated… moved extracellularly and cross-linked

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27
Q

collagen is extremely important in what 3 body structures?

A

skin, teeth, bones

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28
Q

t/f: Vit C is necessary for healthy bones and teeth

A

true!

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29
Q

how are Vit C and Vit E related?

A

Vit C can regenerate Vit E to cont its antioxidant activity (from a-tocopheral radical by donating an e-)

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30
Q

what are the 2 main forms of Vit E we consume? what “subdivisions” do each of these have?

A

tocopherols and tocotrienols… both have alpha, beta, gama, and omega forms…

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31
Q

the alpha form of tocopherols or tocotrienols has R groups off its carbon chain that are ________________s

A

all methyl groups…

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32
Q

what is the structural difference between tocopherols and tocotrienols?

A

tocotrienols have 3 DB in carbon chain off the two rings…

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33
Q

which form of Vit E has the most potent antioxidant activity?

A

alpha tocopherol

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34
Q

how many stereoisomers does alpha tocopherol have?

A

8!

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35
Q

what is the “problem” with synthetic Vit E supplements?

A

contains all 8 stereoisomers of alpha tocopherol but 4 of them are automatically excreted by humans and have no functional effect…

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36
Q

__________ Vit E supplements contain all 8 stereoisomers of alpha tocopherol, while ________ does not contain the 4 stereoisomers that are not maintained by humans

A

“all racemic” v. “natural Vitamin E”

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37
Q

out of all 8 stereoisomers, which form has the most potent antioxidant activity of alpha tocopherol?

A

RRR

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38
Q

what is the RDA for Vit E in both forms?

A

15 mg alpha tocopherol from food or 30 mg synthetic b/c 4 stereosisomers cannot be converted

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39
Q

what are the best dietary sources of Vit E?

A

wheat germ, sunflower seeds, oils(sunflower, safflower), almonds

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40
Q

when eating a good source of Vit E, what is the alpha tocopherol usually bound to? what is this compound called in food(1) and synthesized(2)?

A

fatty acid… called alpha tocopherol ester in food

in supplements: may be alpha tocopherol acetate or succinate

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41
Q

what is the first step of Vit E digestion?

A

fatty acid must be cleaved by a pancreatic esterase to free A.T. –> incorporated into micelle

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42
Q

in the enterocyte, A.T. can be incorporated into what 2 things for export?

A
  1. *chylomicron

2. one of the HDL particles formed in the enterocyte(but not many of these produced here!)

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43
Q

how does Vit E get into tissues?

A

cleaved off chylomicrons or lipoproteins by LPL

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44
Q

once a chylomicron containing a.t. reaches the liver, what are 2 things that can happen to the a.t.?

A
  1. incorporated into lipoprotein and continues into circulation
  2. excreted in bile
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45
Q

what is the main function of Vit E?

A

antioxidant–> neutralizes free radicals by donating an e-

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46
Q

once alpha tocopherol donates an e-, it is called __________. from here, what are the 3 potential pathways for the molecule?

A
  1. another antioxidant like Vit C reduces back to alpha tocopherol
  2. pairs with another alpha tocopherol radical to form dimer that is excreted
  3. donates another e- to another free radical… but cannot be recycled, so also must be excreted
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47
Q

very rarely, a.t. radical is not paired with another e- somehow and it becomes _______________. what is the implication of this situation?

A

becomes a pro-oxidant… must eat a wide variety of antioxidants so they can neutralize each other

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48
Q

t/f: “natural” Vit E supplements are as potent as food Vit E

A

false!

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49
Q

what is the understood units of Vitamin E in the RDA?

A

RRR alpha tocopherol equivalents(TE)

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50
Q

what are the IU–> aTE conversions for synthetic and “natural” supplemented forms?

A

1 IU synthetic–> 0.45 RRR aTE

1 IU “natural”–> 0.67 RRR aTE

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51
Q

what food source has the highest proportion of Vit E as alpha tocopherol, esp. RRR stereoisomer?

A

wheat germ(yum!)

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52
Q

out of the most common oils used in the American diet, which has the most alpha tocopherol?

A

canola oil(over olive oil, soy, corn)

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53
Q

soy and corn oils have mostly ______ tocopherol, which is not as potent

A

gamma

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54
Q

why is Vit E unique among the micronutrients?

A

only has 1 function… act as an antioxidant unlike other micronutrients that usually have several f(x)s

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55
Q

when taking natural v. synthetic Vit E supplements, what is the trend over time in the plasma?

A

with the same dose of each, the natural form will always result in higher plasma levels of circulating alpha tocopherol(remember: all racemic has 1/2 of the stereoisomers simply excreted from the body!)

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56
Q

carotenoids have great __________ capacity

A

antioxidant

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57
Q

t/f: some carotenoids can be converted to Vit A in a healthy person

A

true!

58
Q

what is the difference between Vit A from plant sources and animal sources?

A

plant sources: all carotenoids

animal sources: real Vit A(retinol/things that have activity of Vit A)

59
Q

about _______ carotenoids occur naturally in plants

A

600

60
Q

the most easily converted carotenoid to Vit A is what?

A

beta-carotene

61
Q

what is the difference between preformed Vit A and provitamin A?

A

preformed Vit A is the retinols, while pro-Vit A is carotenes that can be converted to Vit A

62
Q

what are retinoids?

A

umbrella class of molecules similar to retinol from animals(retinol, retinal, retinoic acid)

63
Q

what are the 3 versions of functional Vit A? how do these differ from each other?

A

retinol, retinal, retinoic acid–> differ in the functional groups at the end of their carbon chain

64
Q

we usually eat functional Vit A forms in the form of____________. what is one example of this?

A

retinyl ester… EX. retinal palmitate

65
Q

how are retinyl esters digested?

A

freed to free retinoids by pancreatic esterases

66
Q

when we eat carotenes, how are they converted to Vit A? where does this happen?

A

cleaved in the middle and the L side become Vit A… this occurs in the enterocytes or liver

67
Q

why are carotenes lipid soluble?

A

too large/long chain to be water soluble

68
Q

t/f: some carotenoids cannot be converted to Vit A

A

true!

69
Q

what are 3 carotenoids that ONLY have antioxidant(not retinol) activity

A

lycopene, lutein, zeaxanthin

70
Q

how does the function of lycopene compare to other antioxidants?

A

VERY strong antioxidant

71
Q

what are the best sources of lycopene? (2)

A

tomatoes, pink grapefruit

72
Q

what is the at-home implication of carotenoids being lipid soluble?

A

need to have some fat or oil in cooking to release these antioxidants

73
Q

how must carotenoids and retinoids be absorbed?

A

as free molecules(not bound to fatty acids)–> incorporated into micelles once freed and then diffuse into enterocyte

74
Q

in the enterocyte what happens to carotenoids(3) and retinol(1)?

A

carotenoids: some converted to retinal–> bound to CRBPII–> retinol–> retinyl palmitate OR retinoic acid OR stay the same
retinol: converted to retinyl palmitate

75
Q

what is the difference between how retinoic acid leaves the enterocyte v. retinyl palmitate and carotenoids?

A

retinoic acid secreted into blood and binds to albumin to travel…

retinyl palmitate and carotenoids are incorporated into chylomicrons

76
Q

what must retinyl be bound to in the enterocyte?

A

CRBPII

77
Q

where is Vit A stored in the body? how does this occur? what is the specific cell type in this organ?

A

in the liver cells–> esters on chylomicron cleaved to retinol–> reesterified in liver’s STELLATE(like stellar storage!!) cells

78
Q

when the body needs retinol, how does the liver respond?

A

liver’s STELLATE cells release retinol(cleaves retinyl esters) and binds to RBP(retinol binding protein)–> release complex into blood

79
Q

in the blood the RBP+retinol complex is called ______________. this additionally binds to ___________, making it less likely to be filtered by the ____________ and be excreted

A

called transthyretin, which binds to thyroid hormone to prevent excretion(forms TH-TTR)

80
Q

how does retinol from transthyretin complex (TH-TTR) get into cells?

A

enzymes on cell surfaces to cleave from the hormone and protein

81
Q

in tissues, retinol is taken in, but what must happen in the cells?

A

must be bound to CRBP(cellular retinol binding protein)

82
Q

what two retinoids can interconvert? which conversion is irreversible?

A

retinol and retinal can interconvert, but retinal to retinoic acid is not reversible!

83
Q

name the 3 different categories of functions for the different retinoids

A

retinal: part of rhodopsin in the retina

retinoic acid: cell differentiation and gene expression

retinol: growth, osteoclast activity

84
Q

t/f: the body has innate mechanisms to protect against retinol toxicity

A

true! limits rate of conversion from carotenoids

85
Q

t/f: if someone eats a vegetarian diet, Vit A toxicity is very rare and bone status is not a concern

A

true!

86
Q

what is the Vit A content of most multivitamins?

A

usually a mix of retinol and carotenes

87
Q

what is the implication of Vit A for those living in the arctic?

A

polar bear meat/liver has TONS of retinol, so this specific population is actually at a high risk of toxicity

88
Q

t/f: retinol from food is not sufficient to reach UL

A

true`

89
Q

what are the 3 “compartments” of the retina? what does the lowest level sit next to?

A

photoreceptor, inter photoreceptor space, pigment epithelium(next to blood)

90
Q

when RBP-all trans retinol from the blood enters the pigment epithelium, what does it form? what must it be converted to here?

A

forms CRBP all trans retinol–> converted to 11-cis retinol

91
Q

when CRBP in the pigment epithelium moves to the inter photoreceptor space, what change occurs?

A

binds to IRBP(interphotoreceptor retinol binding protein) instead of CRBP

92
Q

in the photoreceptor, __________ and ___________ combine to form rhodopsin

A

11-cis retinal and opsin

93
Q

when light hits rhodopsin, what happens?

A

opsin splits from the retinal component and the 11 cis retinal becomes ALL-TRANSretinol, then retinal again
**must be transported all the way back through the inter photoreceptor space to the pigment epithelium to be renewed to 11-cis retinal

94
Q

in order for retinoic acid to have gene expression/cell growth regulation f(x), what two forms must be present? what happens to the two of them before their function occurs?

A

9-cis and all -trans retinoic acid must both be present… unbound from their CRBPs and become a dimer

95
Q

in the dimer that moves into the nucleus, all-trans retinoic acid binds to _________ receptors on the DNA, while 9-cis retinoic acid binds to __________ receptors

A

all-trans binds to RAR receptors

9-cis binds to RXR receptors

96
Q

what does binding of the retinoic acid dimer to DNA receptors do?

A

enhances transcription of selected genes with these receptors–> enhances growth and expression of certain proteins

97
Q

if someone has a Vit A deficiency, what might some symptoms be(2)?

A

decreased growth, impaired vision

98
Q

what does RAE stand for?

A

retinoic activity equivalents

99
Q

t/f: some carotenes are more easily converted than others

A

true!

100
Q

t/f: foods fortified with Vit A usually contain the retinol form

A

false- usually contain both retinol and carotenes

101
Q

which converts to retinol more often- dietary or supplemental B-carotene?

A

supplemental

102
Q

1 RAE= ? mcg B carotene from supplements v. dietary

A

1 RAE= 2 mcg supplemental B carotene, but 12 mcg dietary…

103
Q

which of the carotenes in the family convert most efficiently to retinol?

A

Beta

104
Q

1 RAE= ? mcg dietary retinol

A

1 mcg retinol(1:1 conversion rate)

105
Q

what is the conversion between IU of Vit A and RAEs for both supplements and dietary retinol

A
  1. 33 IU= 1 RAE

* *does not matter if IU is from supplement or food! (already factored into calculation of IU)

106
Q

what is the conversion of FOOD B carotene IU to RAE?

A

20 IU food B carotene= 1 RAE

107
Q

t/f: B carotene is a nutrient

A

false! but Vit A is, so B carotene can contribute to meeting our needs for Vit A

108
Q

what is the difference between xenobiotics and free radicals?

A

free radicals are molecules with unpaired electrons; xenobiotics are chemicals or substances with free radicals in them

109
Q

what do xenobiotics and free radicals both do in the body?

A

damage DNA!

110
Q

generally, free radicals and xenobiotics scavenge electrons and cause damage to what types of molecules? what are examples of this in the body?

A

typically molecules with double bonds, like FA tails of phospholipids

111
Q

why are antioxidants necessary to “neutralize” free radicals?

A

antioxidants easily give up e’s to prevent scavenging “damage” of free radicals taking e’s and causing oxidative damage

112
Q

which are more dangerous in the body? dead cells or damaged living cells? explain.

A

damaged living cells–> can still proliferate, creating an army of rogue, damaged cells(ex. cancer)

113
Q

what are 3 characteristics of tumor cells?

A
  1. little contact inhibition
  2. divide uncontrollably
  3. pile up in an unorganized way
114
Q

what are 3 common EXTERNAL sources of free radicals/oxidative stress?

A
  1. city pollution/exhaust
  2. radiation(certain wavelengths like UVB)
  3. cigarette smoke
115
Q

internally, processes that generally produce ________ also often produce free radicals. why does this occur?

A

ATP b/c a lot of the time electron acceptors on the ETC, esp. O becomes a free radical when one electron(unpaired) is accepted

116
Q

to neutralize free radicals formed, like O2* in the ETC, what two steps must occur?(name enzymes)

A

superoxide dismutase converts O2 radical to H202, then catalase or glutathione peroxidase converts to H20

117
Q

what happens if a person does not have enough catalase or glutathione peroxidase in their cells?

A

superoxide dismutase will convert the O2 radical to H202 but this cannot be neutralized to water, so it actually causes more damage and causes MORE free radicals!

118
Q

t/f: SOD is considered part of the antioxidant pathway

A

true… even though it generates another free radical, its one step towards neutralization

119
Q

what does peroxidation mean?

A

means the oxidation of a long chain molecule, like a FA

120
Q

what are two reasons that lipid peroxidation is very concerning?

A
  1. self-propogating(continues indef unless antioxidants neutralize free radicals right away)
  2. auto-catalytic…no enzymes needed for process to occur
121
Q

what element, if unbound, can cause a previously neutralized FA to become a free radical again?

A

Fe in its’ 2+ form

122
Q

the presence of _______, enhances lipid per oxidation by promoting its incorporation into a FA radical

A

O2

123
Q

what is the best prevention for ROS(reactive oxidative stress)?

A

prevention by eating a variety of antioxidants and protein to synthesize antioxidant enzymes: Vit C, Vit E, SOD, glutathione peroxidase, catalase

124
Q

what does the antioxidant enzyme glutathione peroxidase need for structure? what is the best dietary source of this?

A

selenium–> eat Brazil nuts!

125
Q

what is one evolutionary protection v. ROS?

A

compartmentalization: ETC and many metabolic process occur in/across inner mitochondrial membrane, so it’s less likely for unpaired e’s to “sneak out” to other places and cause damage

126
Q

if molecules in cells are highly reactive, they are usually _____________

A

bound to proteins(ex- iron)

127
Q

what is the most prevalent antioxidant in the cell membrane? in the mitochondria?(2)

A

Vit E in cell membrane; glutathione peroxidase and SOD in mitochondria

128
Q

for every location in/outside of the cell, we have more than one antioxidant system. Why is this?

A

so that we are not dependent on one system to neutralize FRs, otherwise if a deficiency/malfunction in that antioxidant occurs, we are up a creek…

129
Q

in cancer prevention, we cannot prevent exposure to carcinogens necessarily, but we can prevent activation… what 2 nutrients are known to prevent this?

A

Vit C and E

130
Q

what prevents an active carcinogen from reaching DNA targets and actually causing damage? (3 dietary examples)

A

phenols
isothiocyanates
flavones

131
Q

if DNA is attacked and mutagenesis occurs, what dietary factors might prevent tumor formation and damaged cell proliferation? (3 examples)

A

phenols
carotenoids
retinoids

132
Q

if retinoids are not antioxidants, how do they help prevent tumor growth?

A

they promote cell differentiation and specified cells are less likely to proliferate if they have mutated than generic stem cells

133
Q

where does detoxification of most xenobiotics occur? how many stages does this process have?

A

in the liver! 2 stages

134
Q

which metabolites of xenobiotics formed in the liver can be excreted?

A

both primary and secondary metabolites

135
Q

if a primary metabolite of a xenobiotic is NOT excreted, what might happen to it?

A

could become a reactive intermediate that causes delayed toxicity, mutations, cancer, etc.

136
Q

stage II detoxification of xenobiotics in the liver is enhanced by dietary intake of ???

A

phytochemicals like phenols, flavones, isothiocyanates, etc.

137
Q

____________ are some of the best sources of isothiocyanates

A

cruciferous veg

138
Q

______ and ______ are some of the best dietary sources of phenols

A

wine and tea/coffee

139
Q

at low levels of oxidative stress, B carotene works as a __________. however, at high exposure to carcinogens/ROS, what happens with B carotene?

A

works as antioxidant at low levels… but at high levels, in vitro data actually shows B carotene increase the amt. of unpaired e’s b/c it can block the effect of other, more potent carotenoids

140
Q

what are the current recommendations re; B-carotene for smokers?

A

do NOT take a B carotene supplement because it has actually been shown to be harmful and prevent antioxidant activity!