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Princeton Bio > Biochemistry 2 > Flashcards

Biochemistry 2 Flashcards

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1
Q

oxidation

A
  • gain oxygen
  • lose hydrogen
  • lose electrons
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2
Q

reduction

A
  • lose oxygen
  • gain hydrogen
  • gain electrons
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3
Q

where does glycolysis occur?

is oxygen needed?

A
  • cytosol

- no

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4
Q

where does the PDC/Krebs cycle occur

is oxygen needed?

A
  • cytosol (prokaryotes)
  • mitochondrial matrix (eukaryotes)
  • indirectly needed
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5
Q

where does the ETC/Ox phos occur?

is oxygen needed?

A
  • cytosol (prokaryotes)
  • inner mitochondrial membrane (eukaryotes)
  • yes directly
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6
Q

enzyme that converts glucose to glucose-6-phosphate

regulation

A
  • hexokinase
  • ATP used
    (-) G-6-P
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7
Q

enzyme that converts fructose-6-phosphate to fructose-1,6-bisphosphate

regulation

A
  • PFK-1
  • first committed step
  • ATP used
    (-) ATP, Citrate
    (+) AMP, F-2,6-bisP
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8
Q

enzyme that converts phosphoenolpyruvate to pyruvate

A
  • pyruvate kinase
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9
Q

PDC

A
  • 2 pyruvate put in
  • 2 acetyl CoA come out; produce 2 NADH and release CO2
  • oxidize pyruvate
  • reduce NAD+
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10
Q

Krebs

A
  • oxidative decarboxylation reactions
  • acetyl-CoA reacts with oxaloacetate - forms citrate with loss of CoA
  • 3 NADH, 1 FADH2 are produced per acetyl-CoA
  • 3 CO2 lost.
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11
Q

2 goals of ETC

A
  • oxidize (empty) the electron carriers

- make usable energy (ATP)

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12
Q

process of ETC

A
  • NADH oxidized at NADH dehydrogenase
  • FADH2 oxidized at coenzyme Q. Electrons from NADH in glycolysis also sent here.
  • electrons flow through cytc reductase, cytc, and cytc oxidase.
  • hydrogens pumped across inner membrane into outer membrane so matrix becomes more basic
  • hydrogens flow through ATP synthase to generate ATP.
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13
Q

number of ATP per NADH

number of ATP per FADH2

A
  • 2.5

- 1.5 (also for NADH from glycolysis)

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14
Q

number of ATP produced in glycolysis

A
  • 4 ATP total
  • 2 ATP needed at beginning
  • 2 ATP net
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15
Q

number of ATP produced in prokaryotes

A

32

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16
Q

number of ATP produced in eukaryotes

A

30

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17
Q

how many hydrogens to produce ATP

A
  • 4
  • 3 per turn
  • 1 to bring Pi in.
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18
Q

fermentation purpose

A
  • regenerates NAD+ (oxidize it)
  • reduce pyruvate
  • allows glycolysis to continue in absence of oxygen.
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19
Q

fermentation process

A
  • pyruvate reduced to ethanol (yeast) or lactic acid (muscle)
  • NAD+ produced.
  • CO2 released.
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20
Q

lactic acid in fermentation

A
  • lactate transported to liver to make pyruvate.
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21
Q

problems with fermentation

A
  • toxic end products

- not enough ATP leads to loss of total energy.

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22
Q

gluconeogenesis

A
  • pyruvate back to glucose
  • when dietary sources of glucose are unavailable and liver is out of glucose and glycogen.
  • occurs in the liver
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23
Q

enzyme that converts pyruvate to OAA

A
  • pyruvate carboxylase

- 2 ATP used

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24
Q

enzyme that converts OAA to PEP

A
  • pyruvate carboxykinase

- 2 GTP used

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25
Q

enzyme that converts f-1,6-bisp to f-6-p

A
  • f-1,6-bisphosphatase

- Pi released

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26
Q

enzyme that converts g-6-p to glucose

A
  • g-6-phosphatase

- Pi released

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27
Q

regulation of f-1,6-bisphosphotase

A

(-) AMP, F-2,6-Bpase

(+) ATP

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28
Q

gluconeogenesis requires

A
  • 4 ATP
  • 2 GTP
  • 2 NADH
29
Q

hormonal regulation of insulin

A
  • blood glucose high
  • stimulates F-2,6-BisP levels
  • stimulates PFK
  • stimulates glycolysis
30
Q

hormonal regulation of glucagon

A
  • blood glucose low
  • inhibits F-2,6-BisP levels
  • inhibits PFK
  • inhibits glycolysis
31
Q

glycogenesis

A
  • formation of glycogen

- stored in liver and lesser in skeletal muscle

32
Q

process of glycogenesis

A
  • glucose to glucose-6-phosphate (by hexokinase) use 1 ATP
  • glucose-6-phosphate to glucose-1-phosphate (by phosphoglucomutase)
  • glucose-1-phosphate to glycogen (glycogen synthase)
  • use of 1 UTP
  • under control of insulin
33
Q

glycogenolysis

A
  • breakdown of glycogen

- use of glucagon and epinephrine

34
Q

process of glycogenolysis

A
  • glycogen to glucose-1-phosphate (glycogen phosphorylase)
  • glucose-1-phosphate - glucose-6-phosphate (phosphoglucomutase)
  • glucose-6-phosphate to glucose by glucose-6-phosphatase
  • under control of glucagon
35
Q

pentose phosphate pathway phases

A
  • oxidative

- nonoxidative

36
Q

oxidative phase

A
  • G6P broken down into ribulose-5-phosphate and 2 NADPH by glucose-6-phosphate dehydrogenase..
  • NADPH feeds back
  • irreversible.
37
Q

nonoxidative phase

A
  • Ribulose-5-phosphate and other carbons broken down to F-6-P and GAP (glycolytic intermediates)
  • also formed ribose-5-phosphate
38
Q

role of NADPH

A
  • reducing power for anabolic reactions (e.g., fatty acid synthesis)
  • reducing power to eliminate free radicals like during detoxification in the liver
  • inability to generate NADPH (G6PDH deficiency) leads to oxidative damage to RBCs and anemia.
39
Q

role of ribulose-5-phosphate

A
  • synthesize nucleotides

- RNA converted to deoxyribose for DNA.

40
Q

breakdown of triglycerides

A
  • broken down into 2 fatty acids and a monoglyceride.

- 3 fatty acids and 1 glycerol

41
Q

fatty acid conversion to acyl-CoA

fatty acid activation in beta oxidation

A
  • begins at outer mitochondrial membrane
  • conversion of fatty acid to acyl-CoA using acyl-CoA synthetase
  • costs 2 ATP
42
Q

beta oxidation of fatty acids

A
  • 4 reactions to cleave bond between alpha and beta carbons to free acetyl-CoA and generate FADH2 and NADH
  • use dehydrogenase to add double bond
  • use thiolase to cleave
  • each round cleaves a 2 carbon acetyl-CoA
  • final round cleaves a 4 carbon acetyl-CoA
43
Q

calculate the number of times through the cycle

A

(#carbons/2) - 1 = that many NADH, FADH2

+1 = that many acetyl-CoA

44
Q

beta oxidation of unsaturated fats

A
  • isomerize the double bond in an additional step if the double bond is in the wrong position.
  • then same thing.
45
Q

fatty acid synthesis starting material

A
  • acetyl-coA + bicarbonate -> malonyl CoA
  • use of 2 ATP
  • by acetyl-CoA carboxylase
46
Q

activation of fatty acid synthesis

A
  • acetyl-CoA + ACP -> acetyl-ACP + CoA (shifted to another part of the enzyme)
  • malonyl-CoA + ACP -> malonyl-ACP + CoA
47
Q

elongation of fatty acid synthesis

A
  • combine acetyl-ACP and malonyl-ACP
  • use of 2 NADPH from PPP to provide energy.
  • addition and loss of CO2 drives unfavorable reactions.
  • For every 2 carbons you add, you need 2 NADPH
48
Q

location of fatty acid oxidation

A
  • mitochondrial matrix
49
Q

fatty acid oxidation linked to

A
  • CoA
50
Q

coenzymes in fatty acid oxidation

A
  • NAD+, FAD
51
Q

energy cost in fatty acid oxidation

A
  • 2 ATP
52
Q

location of fatty acid synthesis

A
  • cytosol
53
Q

fatty acid synthesis linked to

A
  • acyl carrier protein
54
Q

fatty acid synthesis coenzymes

A
  • NADPH
55
Q

energy cost in fatty acid synthesis

A

lots of ATP to convert acetyl-CoA to malonyl-CoA

56
Q

ketogenesis

A
  • during long term starvation, blood glucose levels fall
  • fatty acids oxidized to form acetyl-CoA
  • levels of acetyl-CoA increase
  • some feeds into Krebs
  • others react to form ketone bodies
57
Q

formation of ketone bodies

A
  • two acetyl-CoA combine to form acetoacetate

- aceteoacetate broken down into hydroxybutyrate and acetone.

58
Q

type I diabetes

A
  • no insulin. glucose can’t get into cell
  • patient relies on fatty acid oxidation for acetyl-CoA
  • so many acetyl-CoA. some converted to ketone bodies.
  • DKA - fatigue, confusion, fruity breathe (acetone)
59
Q

ketone bodies

A
  • soluble in blood
  • cross blood bran barrier
  • reconverted to acetyl-CoA for fuel
  • brain cannot use fats as fuel
  • very acidic.
60
Q

glucose high

A
  • make ATP in glycolysis
  • stored as glycogen
  • acetyl CoA from PDC make fatty acids
61
Q

glucose low

A
  • break down glycogen

- gluconeogenesis

62
Q

starved state (all glycogen stores used)

A
  • fatty acid breakdown
  • free fatty acids - Beta oxidation - acetyl-coA - (Krebs and ketone bodies)
  • glycerol - gluconeogenesis
63
Q

what can pass easily through the blood-brain barrier

A
  • small, hydrophobic molecules.

- charged things do not cross membranes.

64
Q

if you lose carbon as CO2

A
  • you will generate a reduced electron carrier such as NADH.
65
Q

primary source of brain during starvation

A
  • ketone bodies being converted to acetyl-CoA
66
Q

protein catabolism

A
  • break down protein from diet into individual amino aids using proteases
  • individual amino acids broken into amino group and carbon skeleton
  • individual amino acids can be used for protein synthesis.
67
Q

amino group used for

A
  • nitrogenous compounds (bases in DNA or RNA)
  • urea cycle (waste product via kidneys)
  • happening in liver
68
Q

carbon skeleton used for

A
  • glucogenic amino acids (used to generate glucose in gluconeogenesis)
  • ketogenic amino acids (lysine and leucine) - converted into acetyl CoA for ketogenesis or Krebs

Princeton Bio (14 decks)

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