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IHN BIOCHEMISTRY FINAL > FINAL: selenium > Flashcards

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

A

selenide

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

A

SECIS

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
Q

Se homeostasis is controlled by

A

kidney

26
Q

se excretion

A

50-60% urinary (as selenosugar)
40-50% feces

27
Q

with high intake __ are secreted in urine as well as selenosugars

A

with high intake di and tri-methyl metabolites are secreted in urine as well as selenosugars

28
Q

3 functions of Se

A
  1. defense against oxidative stress (glutathione peroxidase)
  2. regulate thyroid hormones (5’-DI)
  3. regulate redox status (thioredoxin reductases)
29
Q

glutathione peroxidase functions (2)

A
  1. destroys free radicals
  2. prevent oxidative damage produced by peroxidases
30
Q

4 types of glutathione peroxidases

A

GPX1: cells and plasma
GPX2: GI cells
GPX3: Se transport (milk, plasma) –> kidney
GPX4: IC lipid peroxidase

31
Q

which GPX is most important

A

GPX4 bc it prevents membrane damage

32
Q

5-deiodinases function

A

activate and inactivate thyroid hormones

33
Q

different DIs

A

DI1: liver, produces circulating T3
DI2: brain, pituitary, IC production of T3
DI3: brain, fetus, inactivates T3

34
Q

thioredoxin reductases function

A

regulates IC redox state
synthesis of deoxynucleotides (DNA synthesis)

35
Q

major plasma and EC selenoprotein

A

selenoprotein P

36
Q

selenoprotein P 2 roles

A

Se transport
antioxidant

37
Q

assessing Se

A
  1. enzyme activities (GPX3, GPX1, Selenoprotein P)
  2. GPX activity in RBC (long-term)
  3. Se levels (variable)
38
Q

Se deficiency associated with

A
  1. cancer
  2. cognitive decline
  3. thyroid disease
  4. CVD
39
Q

when to supplement Se

A

only in deficient individuals (not in ppl with normal levels)

40
Q

Keshan disease

A

chronic Se deficiency
children and adolescents in China
focal myocardial necrosis
heart insufficiency
heart enlargement and dysrhythmia
pulmonary edema

IHN BIOCHEMISTRY FINAL (15 decks)

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