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Biochem Flashcards

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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
non classical galactosemia | lack which enzyme?
galactokinase (can't trap galactose)
26
non classical galactosemia | symptoms?
diarrhea, vomiting, dehydration, cataracts | galactosemia and galactosuria
27
with galactosemia, cataracts due to?
aldose reductase converting galactose into galactitol, makes the lense of the eyes cloudy
28
classical galactosemia | lack of which enzyme(s)?
galactose 1-P uridyltransferase (can't get rid of trapped galactose)
29
classical galactosemia | symptoms
diarrhea, vomiting, dehydration, cataracts, LIVER FAILURE + MENTAL RETARDATION (galactosemia and galactosuria)
30
pyruvate dehydrogenase
mitochondria 3 enzymatic reactions irreversible coenzymes require thiamin, lipolic acid, riboflavine (FAD), niacin (NAD)
31
pyruvate dehydrogenase | 3 controls
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
GLYCOLYSIS | glucose
glucose -------> glucose-6-P (uses 1 ATP) (glucokinase/hexokinase)
33
GLYCOLYSIS | glucose-6-P
glucose6P fructose6P | (phosphohexose isomerase)
34
GLYCOLYSIS | fructose-6P
fructose6P -------> fructose 1,6-bisphosphate (uses 1 ATP) (PFK1)
35
GLYCOLYSIS | fructose 1,6, bisphosphate
fructose 1,6 bisP dihydroxyacetoneP + glyceraldehyde3P (aldolase)
36
GLYCOLYSIS | dihydroxyacetoneP glyceraldehyde3P
triosephosphate isomerase
37
GLYCOLYSIS | glyceraldehyde 3P
glyceraldehyde-3P 1,3-bisPglycerate (glyceraldehyde3P dehydrogenase complex) (produces 1 NADH/pyruvate)
38
GLYCOLYSIS | 1,3-bisPglycerate
1,3bisPglycerate 3Pglycerate (phosphoglycerate kinase) (produces 1 ATP / pyruvate)
39
GLYCOLYSIS | 3-Pglycerate
3Pglycerate 2Pglycerate | (phosphoglycerate mutase)
40
GLYCOLYSIS | 2-Pglycerate
2Pglycerate phosphoenolpyruvate | (enolase)
41
GLYCOLYSIS | Penolpyruvate
Penolpyurvate -----> pyruvate (produces 1 ATP/pyruvate) (pyruvate kinase)
42
GLYCOLYSIS | Pyruvate
pyruvate lactate (lactate dehydrogenase) (recyles NADH + H+ into NAD+)
43
GLYCOLYSIS | 3 controlling steps
1. glucokinase/ hexokinase 2. PFK1 3. pyruvate kinase
44
oxaloacetate = catalytic or stochiometric?
catalytic, used over and over again
45
acetyl-CoA = catalytic or stochiometric?
stochiometric = substrate
46
oxaloacetate can be made from?
pyruvate ----> oxaloacetate (pyruvate carboxylase) (uses 1 ATP)
47
KREBS CYCLE | first step
acetyl-CoA + oxaloacetate -----> citrate | (citrate synthase)
48
KREBS CYCLE | citrate
citrate isocitrate | (aconitase)
49
KREBS CYCLE | isocitrate
isocitrate alpha-ketoglutarate (isocitrate dehydrogenase) | produces 1 NADH
50
KREBS CYCLE | alpha-ketoglutarate
alpha-ketoglutarate -----> succinyl-CoA (alpha-ketoglutarate dehydrogenase complex) (produces 1 NADH)
51
KREBS CYCLE | succinyl-CoA
succinyl-CoA succinate (succinyl thiokinase) (produces 1 ATP)
52
KREBS CYCLE | succinate
succinate fumarate (succinate dehydrogenase) (produces 1 FADH)
53
KREBS CYCLE | fumarate
fumarate malate | (fumarase)
54
KREBS CYCLE | malate
malate oxaloacetate (malate dehydrogenase) (produces 1 NADH)
55
KREBS CYCLE | 3 controlling steps?
1. citrate synthase 2. isocitrate dehydrogenase (irreversible, 1st commited step of Krebs cycle) 3. alpha-ketoglutarate dehydrogenase
56
energy production GLYCOLYSIS
glucokinase -1 ATP PFK1 -1 ATP glyceraldehyde 3-P dehy 1 NADH x2 phosphoglycerate kinase 1 ATP x2 pyruvate kinase 1 ATP X2
57
energy production KREBS
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
malonate
poison binds to active site of succinate dehydrogenase and stops the reaction, making Krebs linear and oxaloacetate stoiciometric
59
amphibolic
Krebs cycel can be used anabolically to form amino acid and glucose and catabolically to produce energy from glucose
60
fluoroacetate
poison = fluorocitrate (similar enough to acetate) binds tightly to aconitase and disables it = stops the Krebs
61
ETS (Mitchell's chemiosmotic theory)
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
ETS - cyanide
blocks complex IV
63
ETS - barbital
blocks complex I (protons not pumped out, ATPase stops working)
64
ETS - antimycin A
blocks complex II
65
ETS - oligomycin
blocks ATPase
66
ETS - atratyloside
blocks adamine nucleotide transmutase (transport ADP inside and ATP outside)
67
Name 2 shuttles
glycerophosphate shuttle = 3 ATP | malate aspartate shuttle = 2 ATP
68
pentose shunt - 3 roles?
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
pentose shunt - oxidative part
oxidative = irreversible, very sensitive to NADPH levels, only run if needed glucose-6P + 2 NADP+ ----> ribulose -5P + NADPH + 2 H+
70
pentose shunt - non-oxidative part
reversible 2 roles: produces ribulose5P when needed can work reverse ribulose-5P + ribose5P furctose 6P + glyceraldehyde3P
71
what happens to Krebs, ATPase and ETS if adequate ATP?
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
what happens to Krebs, ATPase and ETS if dinitrophenol (uncoupler)?
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
if cyanidine
shuts down ETS, no reduced cofactors made, no proton gradient
74
reversible enzyme (enolase) controlled by?
substrate/ product
75
2 shuttle systems
glycerophosphate shuttle = 1 FAD | aspartate malate shuttle = 1 NAD

Midterms (5 decks)

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