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Biochemistry FA > Glycolysis, TCA cycle, pyruvate, electron transport chain > Flashcards

Glycolysis, TCA cycle, pyruvate, electron transport chain Flashcards

0
Q

Glycolysis site and all steps (not the enzymes)

A

Cytoplasm
Glucose –> Glucose-6-P –> Fructose-6-P –>
Fructose-1,6-BP –> Gltceraldehyde-3-P –> 1,3 biphosphoglycerate –> 3-phosphoglycerate –> 2-phosphoglycerate –> phosphoenolpyruvate (PEP)
–> Pyruvate

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1
Q

Glycolysis site

A

Cytoplasm

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2
Q

Hexokinase regulation

A

Glucose -6-P -

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3
Q

Glycolysis steps that require ATP

A

Glucose to 6-P- glucose (hexokinase/glucokinase)

Fructose 6-P to fructose -1,6- BP (phosphofrouktokinase

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4
Q

Glucokinase regulation

A

Fructose-6-P -

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5
Q

Glucokinase vs hexokinase about location

A

Glucokinase in liver and β cells of pancreas

Hexokinase in all other tissues

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6
Q

Glycolysis stpes that produce ATP

A

1,3-Biphosphoglycerate to 3-phosphoglycerate (phosphoglycerate kinase)
Phosphoenolpyruvate to pyruvate (pyruvate kinase)

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7
Q

Glycolysis stpes that produce ATP

A

1,3-Biphosphoglycerate to 3-phosphoglycerate (phosphoglycerate kinase)
Phosphoenolpyruvate to pyruvate (pyruvate kinase)

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8
Q

Fructose-6-P to fructose-2,6-BP

A

Phosphofructokinase -2 (activate in fed state)

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9
Q

Fructose -2,6-biphosphate enzymes (and active when)

A
  1. Fructose bisphosphate-2 –> active in fasting

2. Phosphofructokinase-2 –> active in fed

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10
Q

Fructose-2,6-BP to fructose-6-P

A

Fructose bisphosphatase-2 (active in fasting state)

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11
Q

Fructose-2,6-bisphosphate/fasting state

A

Glucagon –> increased cAMP –> increased protein kinase A –> increased fructose bisphosphatase-2, decreased phosphofuctokinase-2,less glycolysis, more gluconeogenesis

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12
Q

Fructose bisphosphate-2 vs Phosphofructokinase-2 according to action and regulation

A

Are the same bifunctional enzyme whose function is reversed by phosphorylation

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13
Q

Fructose-2,6-bisphosphate/fed state

A

Insulin –> decreased cAMP –> decreased protein kinase A –> decreased fructose bisphosphatase-2, increased phosphofuctokinase-2, more glycolysis, less gluconeogenesis

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14
Q

Pyruvate dehydrogenase complex site

What does it link?

A

MITOCHONDRIAL ENZYME complex linking glycolysis and TCA cycle

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15
Q

Pyruvate dehydrogenase complex regulation

A

Active in fed state, not in fasting

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16
Q

Pyruvate dehydrogenase complex reaction

A

Pyruvate + NAD + CoA –> acetyl CoA + CO2 + NADH

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17
Q

Pyruvate dehydrogenase complex contain how many enzymes

A

3

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18
Q

Pyruvate dehydrogenase complex cofactors

A
  1. Pyrophosphate (B1, TPP)
  2. FAD (riboflavin B2)
  3. NAD (B3, niacin)
  4. CoA (B5, pantothenate)
  5. Lipoic acid
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20
Q

Pyruvate dehydrogenase complex activated in by

A
  1. increased NAD+/NADH ratio
  2. increased ADP
  3. Increased Ca2+
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21
Q

The Pyruvate dehydrogenase complex is similar to

A

a-ketoglutarate dehydrogenase complex (same cofactors, similar substrate and action

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21
Q

Lipoic acid inhibitor

A

Arsenic

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22
Q

a-ketoglutarate dehydrogenase complex converts

A

a-ketoglutarate –> succinyl-CoA (TCA)

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23
Q

Arsenic acid inhibits lipoic acids. Findings

A
  1. Vomiting
  2. Rice water stools
  3. Garlic breath
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24
Q

Arsenic action

A

Inhibit glycolysis

Inhibit lipoic acid (dehydrogenase complex)

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25
Q

Pyruvate dehydrogenase complex deficiency causes

A

A buildup of pyruvate that gets shunted to lactate (via LDH) and alanine (via ALT)

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26
Q

Glycolysis pathway (mediators)

A

Glucose glucose-6-P fructose-6-P fructose-1-6-BP glyceraldehyde-3-P 1,3-biphosphoglycerate
2-phosphoglycerate phosphoenolpyruvate –> pyruvate

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28
Q

Pyruvate dehydrogenase complex deficiency treatments

A

Increased intake of ketogenic nutrients (high fat content or increased lysine and leucine

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28
Q

Pyruvate dehydrogenase complex deficiency findings

A
  1. Neurologic defects
  2. Lactic acidosis
  3. Serum alanine starting in infancy
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29
Q

Ketogenic amino acid vs glucogenic aminoacid

A

A ketogenic amino acid is an amino acid that can be degraded directly into acetyl CoA through ketogenesis. This is in contrast to the glucogenic amino acids, which are converted into glucose.

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31
Q

The only purely ketogenic amino acids

A

Lysine

Leucine

32
Q

Pyruvate metabolism deferent pathways (+enzymes and site)

A
  1. Alamine (ALT-B6)-cytoplasm (Cahill cycle)
  2. Oxaloacetate (PC + CO2 + ATP)-mitochondria
  3. Acetyl-CoA (PDH + NAD)-mitochondria
  4. Lactate (LDH +NADH+H)-cytoplasm
32
Q

Pyruvate to alanine (reaction, site, enzyme, function)

A 
Pyruvate  alanine (ALT+B6) cytoplasm
Function: alanine carries amino groups to the liver from muscle (Cahill cycle)
33
Q

Pyruvate pathways function

A
  1. Alanine: carries amino groups to liver from muscle (Cahill cycle)
  2. Oxaloacetate: can replenish TCA cycle or be used in gluconeogenesis
  3. Acetyl-Coa: transition from glycolysis to TCA
  4. Lactic acid: end of anaerobic glycolysis (major pathway of RBC, leukocytes, kidney medulla, lens, testes, cornea) (Cori cycle)
34
Q

Alanine cycle also called

A

Cahill cycle

35
Q

Aminotransferase cofactor

A

B6

36
Q

LDH

A

Lactic acid dehydrogenase

37
Q

Pyruvate to Lactate (reaction, site, enzyme, function)

A

Pyruvate+NADH+H –> lactate+NAD (LDH +B3) cytoplasm

Function: end of anaerobic glycolysis

38
Q

Pyruvate to lactate is major pathway for which tissues

A

RBCs, leukocytes, kidney medulla, lens, testes, cornea

39
Q

Pyruvate to oxaloacetate (reaction, site, enzyme, function)

A

Pyruvate + CO2 + ATP–>oxaloacetate (pyruvate carboxylase + biotin) Mitochondria
Function: oxaloacetate can replenish TCA cycle or cycle or be used in gluconeogenesis

40
Q

Pyruvate to acetyl-Coa (reaction, site, enzyme, function)

A

Pyruvate+NAD –> acetyl-CoA + CO2 + NADH+H (pyruvate dehydrogenase, B1, B2, B3, B5, lipoic acid) Mitochondria
Function: transition from glycolysis to the TCA cycle

42
Q

TCA cycle produces

site?

A

3 NADH, 1 FADH2, 2 Co2, 1 GTPper acetyl coa (2 x everything per glucose) –> 10 ATP / acetyl coa
site mitochondria

43
Q

TCA cycle - every step

A
  • Acetyl-CoA (2C) + Oxaloacetate (4C) –> Citrate (6C) (Citrate synthase)
  • Citrate –> cis-Aconitate –> Isocitrate
  • Isocitrate –> a-KG (5C) + CO2 + NADH (isocitrate dehydrogenase)
  • a-KG (5C) –> Succinyl-Coa (4C) + CO2 + NADH (a-KG dehydrogenase
  • Succinyl-Coa (4C) –> Succinate + CoA + GTP
  • Succinate –> Fumarate + FDH2
  • Fumarate –> Malate –> Oxaloacetate + NADH
44
Q

A-ketogluterate dehydrogenase cofactors

A

Same as the pyruvate dehydrogenase

B1, B2, B3, B5, lipoic acid

44
Q

Citrine synthase regulator

A

ATP-

45
Q

pyruvate dehydrogenase regulator

A
  • ATP
  • acetyl CoA
  • NADH
46
Q

Isocitrate dehydrogenase regulator

A

ATP-
NADH-
ADP+

48
Q

A-ketoglorate dehydrogenase regulators

A

Succinyl CoA -
NADH-
ATP-

48
Q

NADH production reaction of TCA

A

Isocitrate–> a ketoglutorate + CO2 + NADH
a ketoglutorate–> succinyl coa + CO2 + NADH
Malate–> oxaloacetete + NADH

49
Q

Irreversible enzymes of TCA cycle

A
  1. Pyruvate dehydrogenase
  2. Isocitrate dehydrogenase
  3. a ketoglutorate dehydrogenase
  4. Citrate synthase
50
Q

FAD2 production reaction of TCA

A

Succinate –> fumareta + FAD2

51
Q

GTP production reaction of TCA

A

Succinate CoA –> succinyl + CoA + GTP

52
Q

NADH Electrons from glycolysis enter mitochondria via

A
  1. Malate-aspartate shuttle

2. Glycerol phosphate shuttle

53
Q

FADH2 electrons are transferred to

A

Complex II (at a lower energy level than NADH

54
Q

NADH electrons are transferred to

A

Complex I

55
Q

Complex II name

A

Succinate dehydrogenase

56
Q

Proton gradient purpose

A

Is coupled to oxidative phosphorylation, it drives the production of ATP

57
Q

The passage of electrons to intermembrane matrix through….results in the formation of a…

A

Complex I, Complex III, and Complex IV

Proton gradient

58
Q

Which complex of electron transport chain produce water

A

Complex IV

1/2O2 + 2H H2O

59
Q

Which complex of electron transport chain produce ATP

A

Complex V

60
Q

H+ go to mitochondrial matrix through

A

Complex V

61
Q

Molecule between complex II and III

A

CoQ

62
Q

Molecule between complex III and IV

A

Cytochrome c

63
Q

Complex I inhibitor

A

Rotenone

64
Q

Complex III inhibitor

A

Antimycin A

65
Q

Complex IV inhibitor

A

Cyanide

CO

66
Q

Complex V inhibitor

A

Oligomiycin

67
Q

Electron transport inhibitors

A

Rotenone, cyanide, antimycin A, CO

Directly inhibit electron transport, causing a decreased proton gradient and block of ATP synthesis

68
Q

ATP produce via ATP synthase in oxidative phosphorylation

A

2,5 ATP per NADH

1,5 ATP per FADH2

69
Q

ATP synthase inhibitors

A

Oligomycin
Directly inhibit mitochondrial ATP synthase , causing an increased proton gradient. No ATP is produce because electron transport stop

70
Q

Electron transport chain-uncoupling agent mechanism of action

A

Imcreased permeability of membrane, causing a decreased proton gradient and increased O2 consumption. ATP synthesis stops, but electron transport continues. Produces heat

72
Q

Electron transport chain-uncoupling agents

A

2,4-Dinitrophenol (used illicitly for weight loss)
Aspirin (fevers often occur after aspirin overdose)
Thermogenin in brown fat

73
Q

phosphofructokinase - 1 in glycolisis - mechanism of action and regulation

A

Fructose-6-P –> Fructose - 1,6-BP
+: AMP, fructose-2,6-BP
-: ATP, Citrate

74
Q

Pyruvate kinase regulation

A
  1. Fructose 1,6 BP +
  2. ATP -
  3. Alanine -
75
Q

Inhibitors of every step of electron transport chain and oxidative phosphorylation

A 
Complex I --> rotenone 
Complex III --> Antimycin A 
Complex IV --> Cyanide, CO 
Complex V --> oligomycin 
Uncoupling agents --> Dinitrophenol, aspirin, thermogenein
76
Q

2,4-Dinitrophenol - clinical use

A

illicitly for weight loss

Biochemistry FA (16 decks)

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