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Midterms > Biochem > Flashcards

Biochem Flashcards

1
Q

bond - sucrose

A

alpha 1, beta 2

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2
Q

bond - lactose

A

beta 1,4

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3
Q

bond - trehalose

A

alpha 1,1

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4
Q

bond - maltose

A

alpha 1,4

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5
Q

bond - isomaltose

A

alpha 1,6

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6
Q

reducing sugars

A

lactose, isomaltose, glucose, galactose

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7
Q

non-reducing sugars

A

sucrose, trehalose, raffinose

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8
Q

amylase breaks bonds?

A

alpha 1,4

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9
Q

isomaltase only one to break bonds?

A

alpha 1,6

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10
Q

results digestion alpha-amylase

A

40% maltose
30% alpha-dextrins
25% maltotriose
5% glucose OGS

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11
Q

membrane-bound complexes

A 
sucrase isomaltase complex (jejunum)
glucoamylase complex (ilem)
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12
Q

enantiomer

A

D and L glucose (mirror)

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13
Q

epimer

A

glucose and galactose

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14
Q

anomer

A

alpha and beta glucose

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15
Q

2 enzymes both cytoplasm and mitochondria

A

malate dehydrogenase
aspartate transaminase

and glycerol-3-P dehydrogenase too?

(shuttle)

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16
Q

3 controlling steps of glycolysis

A
  1. glucokinase/hexokinase
  2. PFK1
  3. pyruvate kinase
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17
Q

hexokinase vs. glucokinase

A

hexokinase = muscle and brain
non inducible, sensitive to cell’s needs, works best at low concentrations, inhibited by products (G6P), works with other sugars

glucokinase = liver, very sensitive to dietary glucose, works very quickly, inducible by insulin, only with glucose

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18
Q

PFK1 importance?

A

sensitive to energy charge of the cell

activated by fructose 2,6-bisphosphate and high AMP

inhibited by high ATP

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19
Q

first irreversible step unique glycolytic pathway

A

PFK1

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20
Q

mannose

A

importance for synthesis of glycoproteins
can be made from glucose
no enzyme to convert mannose6-P since mannose itself not needed
hexokinase can convert mannose 6-P into fructose 6-P, then fit in the glycolytic pathway

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21
Q

what enzyme does fructose bypass

A

PFK1

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22
Q

fructose metabolism

A

only in liver
converted to fructose 1-P and directly converted with aldolase to dihydroxyacetoneP and glyceraldehyde
this glyceraldehyde is not trapped and need to be phosphorylated to glyceraldehyde3P
insulin not required
easier to make pyruvate from fructose rather than convert to glucose

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23
Q

galactose conversion to glucose

A

not so easy, but primordial (infants)
trapped in the cell using galactokinase
galactose 1-P uridyltransferase does 2 things
1. take UMP from UDP to form glucose 1-P (de energizing)
2. adding this UMP and add it to galactose 1-P (energizing)

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24
Q

interconversion of galactose 1-P into glucose 1-P only possible when?

A

molecules energized

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25
Q

non classical galactosemia

lack which enzyme?

A

galactokinase (can’t trap galactose)

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26
Q

non classical galactosemia

symptoms?

A

diarrhea, vomiting, dehydration, cataracts

galactosemia and galactosuria

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27
Q

with galactosemia, cataracts due to?

A

aldose reductase converting galactose into galactitol, makes the lense of the eyes cloudy

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28
Q

classical galactosemia

lack of which enzyme(s)?

A

galactose 1-P uridyltransferase (can’t get rid of trapped galactose)

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29
Q

classical galactosemia

symptoms

A

diarrhea, vomiting, dehydration, cataracts, LIVER FAILURE + MENTAL RETARDATION
(galactosemia and galactosuria)

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30
Q

pyruvate dehydrogenase

A

mitochondria
3 enzymatic reactions
irreversible
coenzymes require thiamin, lipolic acid, riboflavine (FAD), niacin (NAD)

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31
Q

pyruvate dehydrogenase

3 controls

A
  1. direct inhibition by product (NADH and acetyl CoA)

2 and 3. covalent modification
inhibited by pyruvate dehydrogenase kinase (add a phosphate) when ATP, NADH and acetyl-CoA levels raise (no energy needed) and activated by pyruvate dehydrogenase phosphatase (remove the P) when pyruvate and Ca levels raise

32
Q

GLYCOLYSIS

glucose

A

glucose ——-> glucose-6-P
(uses 1 ATP)
(glucokinase/hexokinase)

33
Q

GLYCOLYSIS

glucose-6-P

A

glucose6P fructose6P

(phosphohexose isomerase)

34
Q

GLYCOLYSIS

fructose-6P

A

fructose6P ——-> fructose 1,6-bisphosphate
(uses 1 ATP)
(PFK1)

35
Q

GLYCOLYSIS

fructose 1,6, bisphosphate

A

fructose 1,6 bisP dihydroxyacetoneP + glyceraldehyde3P (aldolase)

36
Q

GLYCOLYSIS

dihydroxyacetoneP glyceraldehyde3P

A

triosephosphate isomerase

37
Q

GLYCOLYSIS

glyceraldehyde 3P

A

glyceraldehyde-3P 1,3-bisPglycerate
(glyceraldehyde3P dehydrogenase complex)
(produces 1 NADH/pyruvate)

38
Q

GLYCOLYSIS

1,3-bisPglycerate

A

1,3bisPglycerate 3Pglycerate
(phosphoglycerate kinase)
(produces 1 ATP / pyruvate)

39
Q

GLYCOLYSIS

3-Pglycerate

A

3Pglycerate 2Pglycerate

(phosphoglycerate mutase)

40
Q

GLYCOLYSIS

2-Pglycerate

A

2Pglycerate phosphoenolpyruvate

(enolase)

41
Q

GLYCOLYSIS

Penolpyruvate

A

Penolpyurvate —–> pyruvate
(produces 1 ATP/pyruvate)
(pyruvate kinase)

42
Q

GLYCOLYSIS

Pyruvate

A

pyruvate lactate
(lactate dehydrogenase)
(recyles NADH + H+ into NAD+)

43
Q

GLYCOLYSIS

3 controlling steps

A
  1. glucokinase/ hexokinase
  2. PFK1
  3. pyruvate kinase
44
Q

oxaloacetate = catalytic or stochiometric?

A

catalytic, used over and over again

45
Q

acetyl-CoA = catalytic or stochiometric?

A

stochiometric = substrate

46
Q

oxaloacetate can be made from?

A

pyruvate —-> oxaloacetate
(pyruvate carboxylase)
(uses 1 ATP)

47
Q

KREBS CYCLE

first step

A

acetyl-CoA + oxaloacetate —–> citrate

(citrate synthase)

48
Q

KREBS CYCLE

citrate

A

citrate isocitrate

(aconitase)

49
Q

KREBS CYCLE

isocitrate

A

isocitrate alpha-ketoglutarate (isocitrate dehydrogenase)

produces 1 NADH

50
Q

KREBS CYCLE

alpha-ketoglutarate

A

alpha-ketoglutarate —–> succinyl-CoA
(alpha-ketoglutarate dehydrogenase complex)
(produces 1 NADH)

51
Q

KREBS CYCLE

succinyl-CoA

A

succinyl-CoA succinate
(succinyl thiokinase)
(produces 1 ATP)

52
Q

KREBS CYCLE

succinate

A

succinate fumarate
(succinate dehydrogenase)
(produces 1 FADH)

53
Q

KREBS CYCLE

fumarate

A

fumarate malate

(fumarase)

54
Q

KREBS CYCLE

malate

A

malate oxaloacetate
(malate dehydrogenase)
(produces 1 NADH)

55
Q

KREBS CYCLE

3 controlling steps?

A
  1. citrate synthase
  2. isocitrate dehydrogenase (irreversible, 1st commited step of Krebs cycle)
  3. alpha-ketoglutarate dehydrogenase
56
Q

energy production GLYCOLYSIS

A

glucokinase -1 ATP
PFK1 -1 ATP
glyceraldehyde 3-P dehy 1 NADH x2
phosphoglycerate kinase 1 ATP x2
pyruvate kinase 1 ATP X2

57
Q

energy production KREBS

A

pyruvate dehydrogenase 1 NADH x2
isocitrate dehydrogenase 1 NADH x2
alpha-ketoglutarate dehydro 1 NADH x2
succinate thiokinase 1 ATP x 2
succinate dehydrogenase 1FADH X2
malate dehydrogenase 1 NADH x2

58
Q

malonate

A

poison binds to active site of succinate dehydrogenase and stops the reaction, making Krebs linear and oxaloacetate stoiciometric

59
Q

amphibolic

A

Krebs cycel can be used anabolically to form amino acid and glucose

and catabolically to produce energy from glucose

60
Q

fluoroacetate

A

poison = fluorocitrate (similar enough to acetate) binds tightly to aconitase and disables it = stops the Krebs

61
Q

ETS (Mitchell’s chemiosmotic theory)

A

outward pumping of hydrogen ions from mitochondrial matrix
oxidation of NADH and FADH2 in mitochondria by ETS
series of oxidized and reduced steps
ATPase is the only way to pump hydrogen ions back in
3 complexes (coQ10, iron, oxygen)

62
Q

ETS - cyanide

A

blocks complex IV

63
Q

ETS - barbital

A

blocks complex I (protons not pumped out, ATPase stops working)

64
Q

ETS - antimycin A

A

blocks complex II

65
Q

ETS - oligomycin

A

blocks ATPase

66
Q

ETS - atratyloside

A

blocks adamine nucleotide transmutase (transport ADP inside and ATP outside)

67
Q

Name 2 shuttles

A

glycerophosphate shuttle = 3 ATP

malate aspartate shuttle = 2 ATP

68
Q

pentose shunt - 3 roles?

A
  1. used to produce NADPH (requires for fatty acid synthesis, cytochrome P450 detox, cholesterol synthesis)
  2. gives 5-carbon sugar (ribulose/ribose)
  3. converts 5-carbon sugar into glycolytic intermediates

important to provide nucleotide for protein synthesis

69
Q

pentose shunt - oxidative part

A

oxidative = irreversible, very sensitive to NADPH levels, only run if needed

glucose-6P + 2 NADP+ —-> ribulose -5P + NADPH + 2 H+

70
Q

pentose shunt - non-oxidative part

A

reversible
2 roles: produces ribulose5P when needed
can work reverse
ribulose-5P + ribose5P furctose 6P + glyceraldehyde3P

71
Q

what happens to Krebs, ATPase and ETS if adequate ATP?

A

adequate energy
inhibit Krebs and slows down ETS
citrate synthase and isocitrate dehydrogenase are inhibited by ATP
if ATP is high, hydrogen ions build up outside mitochondria and ETS shut down
ATPase also inhibited by adequate ATP
Krebs, ETS and ATP levels are closely interrelated
If adequate ATP, extra glucose = glycogenesis and fatty acid synthesis

72
Q

what happens to Krebs, ATPase and ETS if dinitrophenol (uncoupler)?

A

makes system less efficient
carries hydrogen inside mitochondria bypassing ATPase, making ETS increase its activity to try to pump H+ out, speeding up the Krebs cycle at the same time
= more fuel oxidation without generating ATP
= weight loss
generates a lot of heat, can be problematic for homeostasis and can also damage the liver (responsible for processing dinitrophenol)

73
Q

if cyanidine

A

shuts down ETS, no reduced cofactors made, no proton gradient

74
Q

reversible enzyme (enolase) controlled by?

A

substrate/ product

75
Q

2 shuttle systems

A

glycerophosphate shuttle = 1 FAD

aspartate malate shuttle = 1 NAD

Midterms (5 decks)

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