FINAL: selenium Flashcards

1
Q

bioactive form of selenium

A

selenoproteins

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2
Q

2 selenoamino acids present in proteins

A
  1. selenomethionine (plants)
  2. selenocytsteine (animals)
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3
Q

what do selenoamino acids make

A

selenoproteins

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4
Q

Se RDA increases with

A

age
pregnancy
lactation

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5
Q

Se food source

A

brazil nuts
fish
meat

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6
Q

can Se lead to toxicity

A

YES
only Se and vit A

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7
Q

levels of Se in men and women are same but,

A

women consume less, so they must have better control

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8
Q

Se toxicity inhibits

A

protein synthesis

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9
Q

__% absorption of Se in gut

A

80-98% absorption of Se in gut

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10
Q

selenium absorber

A

SLC26

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11
Q

Se absorption in gut

A
  1. selenate and selenite enter SLC26
  2. Se-cysteine (animals) and Se-methionine (plants) enter B0AT and rBAT
  3. some to functional pool, rest to portal circulation
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12
Q

B(0)AT is dependent on

A

Na

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13
Q

__ uptakes 50% Se

A

liver uptakes 50% Se

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14
Q

most Se in post-hepatic circulation is transported by __

A

most Se in post-hepatic circulation is transported by selenoprotein P

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15
Q

selenoprotein P is made in __ and secreted into __

A

selenoprotein P is made in liver and secreted into circulation

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16
Q

elemental selenium in body is called

A

selenide

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17
Q

what is the main transporter of selenium in circulation

A

selenoprotein P

18
Q

SEC =

A

selenocysteine

19
Q

selenide can be converted to __ by __

A

selenide can be converted to selenophosphate by selenophosphate synthetase

20
Q

All selenium we consume is converted to

21
Q

selenide pathway

A
  1. selenide to selenophosphate
  2. selenophosphate uses tRNA for Serine to become selenocysteine
  3. selenocystine is used in translation and protein synthesis
22
Q

selenoprotein synthesis trxn

A

UGA (normally a stop codon) codes for seleno-cysteine when SECIS is present

23
Q

what must be present for UGA to not be read as a stop codon

24
Q

high selenium is found in what organs and why

A
  1. thyroid bc thyroid hormones
  2. liver bc 1) it directs Se to where it needs to go and 2) liver has DI1 which makes T3
25
Se homeostasis is controlled by
kidney
26
se excretion
50-60% urinary (as selenosugar) 40-50% feces
27
with high intake __ are secreted in urine as well as selenosugars
with high intake **di and tri-methyl metabolites** are secreted in urine as well as selenosugars
28
3 functions of Se
1. defense against oxidative stress (glutathione peroxidase) 2. regulate thyroid hormones (5'-DI) 3. regulate redox status (thioredoxin reductases)
29
glutathione peroxidase functions (2)
1. destroys free radicals 2. prevent oxidative damage produced by peroxidases
30
4 types of glutathione peroxidases
GPX1: cells and plasma GPX2: GI cells GPX3: Se transport (milk, plasma) --> kidney GPX4: IC lipid peroxidase
31
which GPX is most important
GPX4 bc it prevents membrane damage
32
5-deiodinases function
activate and inactivate thyroid hormones
33
different DIs
DI1: liver, produces circulating T3 DI2: brain, pituitary, IC production of T3 DI3: brain, fetus, inactivates T3
34
thioredoxin reductases function
regulates IC redox state synthesis of deoxynucleotides (DNA synthesis)
35
major plasma and EC selenoprotein
selenoprotein P
36
selenoprotein P 2 roles
Se transport antioxidant
37
assessing Se
1. enzyme activities (GPX3, GPX1, Selenoprotein P) 2. GPX activity in RBC (long-term) 3. Se levels (variable)
38
Se deficiency associated with
1. cancer 2. cognitive decline 3. thyroid disease 4. CVD
39
when to supplement Se
only in deficient individuals (not in ppl with normal levels)
40
Keshan disease
chronic Se deficiency children and adolescents in China focal myocardial necrosis heart insufficiency heart enlargement and dysrhythmia pulmonary edema