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Term 1 > Biochemistry - Cellular respiration > Flashcards

Biochemistry - Cellular respiration Flashcards

1
Q

What are the 2 functional groups of monosaccharides?

A

Aldose (H - C = O) & Ketose (C = O)

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2
Q

Who reacts faster – aldose or ketose?

A

Aldose

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3
Q

Give examples of trioses: aldose and ketose.

A

Ald- glyceraldehyde; Ket- dihydroxyacetone

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4
Q

Give example of tetrose aldose.

A

Erythrose

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5
Q

Give exampels of pentose aldoses and ketoses.

A

Ald- Ribose, xylose; Ket- Ribulose, xyluose

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6
Q

Give examples of hexose aldoses and ketoses.

A

Ald- Glucose, galactose, mannose; Ket- fructose

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7
Q

Give example of heptose ketose

A

Sedoheptulose

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8
Q

Sugar in the urine is a result of:

A

DM, fructosuria, glaactosuria

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9
Q

Give an example of a polyol and state its importance.

A

Sugar alcohol, sorbitol; can cause damage in DM; incorporates in nerves, lens of eye, retina

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10
Q

Define an epimer

A

Same chemical formula, -OH in different position

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11
Q

Give 2 sets of epimers and state the epimerization

A

Glucose/Galactose (C4 epimers); Glucose/Mannose (C2 epimers)

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12
Q

Give 3 examples of brush border disaccharides. State whether they are reducing or non-reducing sugars.

A

Lactose - Glu-Gal (beta-1-4 glycosidic)
Sucrose - Glu-Fru (C1-C2) *NON-reducing
Maltose - Glu-Glu (alpha-1-4 glycosidic)

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13
Q

T/F Fructose is a ketohexose

A

True

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14
Q

What is HFCS?

A

High fructose corn syrup (> 50% fructose in sugar – ingested in the body as a mixture)

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15
Q

What is glycogen? How are units linked?

A

Storage glucose / homopolysaccharide
Linear: alpha-1-4 glycosidic
Branched: alpha-1-6 glycosidic

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16
Q

What is starch? How are units linked?

A

Homopolysaccharide; found in plants
Amylose - linear alpha-1-4 glycosidic
Amylopectin- linear alpha-1-4 & branched alpha-1-6 glycosidic

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17
Q

What is dietary fiber?

A

Undigestable cellulose (beta-1-4 linkages – lactase CANNOT break this down); maintains normal peristalsis

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18
Q

Differentiate between hexokinase and glucokinase.

A

HK: Low Km, high affinity for glucose; most cells express HK

GK: only in liver and beta-pancreas; high Km, low affinity for glucose (only active at high [glucose])

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19
Q

What inhibits HK?

A

A high [G-6-P]

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20
Q

Who has a higher Km: HK or GK?

A

GK – has a low affinity for glucose and is only active in the liver and beta-pancreas at high [glucose]

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21
Q

Increased ATP will increase/decrease the activity of PFK?

A

Decrease

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22
Q

Differentiate between insulin & glucagon’s impact on PFK.

A

Insulin - high glucose, de-phosphorylate PFK-2 to increase the formation of F-2,6-bisphosphate, which activates PFK-1

Glucagon - phospohrylates PFK-1, which stimulates fructose 2,6 bi-phosphatase (decreased levels of fructose-2,6,-biphsosphate); activates fructose 1,6,-biphosphatase

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23
Q

Where does carbohydrate digestion begin?

A

Mouth - salivary alpha-amylase

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24
Q

What is the fate of salivary alpha-amylase in the stomach?

A

Inactivated by acidic lumen of stomach

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25
Q

Where does lipid digestion begin?

A

Mouth - lingual lipase

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26
Q

What is the fate of lingual lipase in the stomach?

A

Active, along with gastric lipase

* Degradation of TAG’s (medium-chain) and sends directly to the portal vein

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27
Q

Where does glycolysis take place?

A

The cytosol

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28
Q

What is the overall goal of glycolysis?

A

Oxidize glucose to 2 molecules of pyruvate

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29
Q

What are the 3 irreversible steps of glycolysis?

A
  1. Glucose –> G-6-P (GK/HK)
  2. F-6-P –> F, 1,6 bis-phosphate (PFK-1)
  3. Phosphoenolpuyruvate –> Pyruvate (PK)
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30
Q

How many substrate-level phosphorylations are present in glyolysis?

A
  1. 1,3-BPG –> 3-phosphoglycerate (phosphoglycerate kinase)

2. Phosphoenolpuyruvate –> Pyruvate (PK)

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31
Q

What does arsenate inhibit along the glyocolytic pathway?

A

Glyeraldehyde-3-phosphate-dehydrogenase

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32
Q

What does fluoride inhibit along the glycolytic pathway?

A

Enolase

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33
Q

Where does pyruvate dehydrogenase take place?

A

Mitochondrial matrix

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34
Q

Briefly describe the 3 stages of metabolism.

A
  1. Large molecules –> building block molecules (digestion)
  2. Common degradation product (pyruvate/acetyl-coA)
  3. Simple, small products of catabolism
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35
Q

What are the 4 fates of pyruvate?

A
  1. Lactate
  2. Acetyl coA
  3. Oxaloacetate
  4. Alanine
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36
Q

What is the link between glycolysis and the TCA cycle?

A

Pyruvate dehydrogenase complex

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37
Q

What type of reaction is pyruvate –> acetyl-CoA?

A

Decarboxylation

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38
Q

What are the reactants and products of PDC?

A
  1. 2 Pyruvate

2. 2 acetyl-CoA & 2 NADH

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39
Q

What are the 3 enzymes required for PDC?

A
  1. PDH
  2. Dihydrolipoyl dehydrogenase
  3. Dihydrolipol transacetylase
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40
Q

What are the 2 regulatory proteins for PDC?

A
  1. Protein kinase

2. Protein phosphatase

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41
Q

What are the 5 co-enzymes required in PDC?

A
  1. CoA - vitamin B5
  2. FAD - riboflavin / vitamin B2
  3. NAD+ - niacin / vitamin B3
  4. TPP
  5. Lipoic acid (non-vitamin derivative)
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42
Q

Do the following stimulate or inhibit PDH?

  1. Dephosphorylation
  2. Insulin in adipocytes and liver
  3. Catecholamines in cardiac muscle
  4. Ca in skeletal muscle
A

Stimulate

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43
Q

Do the following stimulate or inhibit PDH?

  1. Phosphorylation
  2. Acetyl CoA
  3. ATP
  4. NADH
A

Inhibit

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44
Q

Acetyl coA can be derived from two other processes aside from PDH. What are they?

A
  1. Lipolysis

2. Proteolysis

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45
Q

What are synonyms for TCA cycle?

A
  1. Tricarboxylic acid cycle
  2. Krebs cycle
  3. Citric acid cycle
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46
Q

How many ATP are generated for each molecule of pyruvate sent to PDH?

A

3 ATP, or 1 NADH (3 ATP * 2 b/c we send 2 pyruvates)

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47
Q

Which are the 4 regulated enzymes in TCA?

A
  1. Citrate synthase
  2. Isocitrate dehydrogenase
  3. alpha-KG dehydrogenase
  4. Succinate dehydrogenase
48
Q

What are the products of one cycle of the TCA?

A
  1. 3 NADH
  2. 1 GTP
  3. 1 FADH2
  • This is 12 ATP per each acetyl coA
49
Q

How many ATP produced per NADH?

A

3

50
Q

How many GTP produced per ATP?

A

1

51
Q

How many FADH2 produced per ATP?

A

2

52
Q

In general, what stimulates TCA cycle and what inhibits it?

A

Stimulate – low energy

Inhibit – high energy

53
Q

A high ratio of ATP:ADP will stimulate/inhibit the TCA cycle?

A

Inhibit

54
Q

What are the ATP totals for glycolysis?

A

8 ATP (2 pyruvates)

55
Q

What are the ATP totals for PDH?

A

6 ATP (2 pyruvates)

56
Q

What are the ATP totals for TCA cycle?

A

24 ATP (2 acetyl-co-A’s)

57
Q

Kearns-Sayre syndrome, MELAS syndrome, and MERRF syndrome are…

A

mitochondiral myopathies

58
Q

What is Leber’s Hereditary Optic Neuropathy?

A

Inherited mitochondrial disease

  • Affect TCA, ETC, beta-oxidation FA’s
  • Defect in NADH dehydrogenase (ETC)
59
Q

Malonate inhibits

A

Succinate dehydrogenase

60
Q

Niacin is vitamin ____

A

B3

61
Q

Riboflavin is vitamin ______

A

B2

62
Q

Thiamine is vitamin ____

A

B1

63
Q

Pantothenate is another name for _____

A

coA

64
Q

Cobalamin is vitamin ______

A

B12

65
Q

Fluroacetate inhibits what in TCA cycle?

A

Acotinase

66
Q

Arsenic poisoning affects this in the PDH

A

Results from its binding to lipoic acid which is needed for the activity of dihydrolipoyl transacetylase

67
Q

What is Werneke-Korsakoff syndrome?

A
  • Thiamine deficiency
  • Ataxia, opthalmolplagia
  • Memory loss
  • Cerebral hemorrhage
  • Common in alcoholics, malnourished individuals
    Can result in: heart failure, decrease ATP, increased cardiac output
    Other thiamine-requiring enzymes: alpha-ketogluterate DH & branched-chain alpha-ketoacid DH
68
Q

What is congenital lactic acidosis (pyruvate dehydrogenase deficiency)

A

Metabolic: increase in pyruvate with concomitant increase in lactic acid and alanine; decrease production in acetyl coA; severe reduction in ATP production
* Loss of 30 ATP from PDH  TCA!

Clinically: lactic acidosis, neuro defects, myopathy, usually fatal

69
Q

What is the Warburg effect in cancer?

A

Most cancer cells use glycolysis as main source of ATP

  • A glucose FDG (flurodeoxyglucose) is used for PET scanning
  • Tumor cells take up FDG
  • Pharm. Inhibitors of glycolysis explored as therapeutic agents
70
Q

What is Leigh Disease?

A

Inherited pyruvate dehydrogenase deficiency

71
Q

What is the most common glycolytic enzyme deficiency?

A

G-6-P deficiency

72
Q

What results clinically secondary to pyruvate kinase deficiency?

A

Hemolytic anema

73
Q

What results from inherited GK deficiency?

A

Rare form of inherited DM and elevated blood glucose

-Beta-cells of pancreas cannot respond to high blood glucose levels

74
Q

Taking too many antacids can result in…

A

Reduction of protein digestion in the stomach b/c at an increased pH, the gastric HCl will not be active to denature protein

75
Q

A high carbohydrate diet will lead to…

A

An increase in FA synthesis in the liver, increased fat deposits

76
Q

What is autocatyltic pancreatitis?

A

Trypsin is abnormally active in the pancreas; it abnormally activates other pancreatic zymogens

highly active proteases and phospholipase A will destroy proteins and lipids in the membrane of the pancereas and at the pancreatic duct

  • Etiology: gallstones/tumor (inc. ALP)
  • Hyper TAGemia
  • ETOH abuse
  • Serum markers: amylase & lipase
77
Q

What is cholelithiasis?

A

Cholesterol gallstone disease

  • Can lead to pancreatitis
  • Etiology: decreased bile salts and phosphatidylcholine in bil
  • Increased biliary cholesterol secretion
78
Q

What is steatorrhea and what does it result from?

A

Fatty feces

  1. Lack conjugated bile salts
  2. Defects in pancreatic juices
  3. Defective mucosa
  4. Short bowel syndrome
79
Q

What is celiac disease?

A

Gluten intolerance

80
Q

What are the 3 forms of lactose intolerance?

A

Congenital - can be serious (milk for the infants!!!)
Primary - Lactase activity down to 10%
Secondary - damage to intestinal mucosa

81
Q

Describe cystic fibrosis.

A

Defective CFTR
1. Dec. reabsorption of sweat (salty sweat test)
2. Dec expulsion of Cl- in lungs/panc; mucous becomes very thick (water usually follows Cl-
 Can lead to fibrosis of the pancreas, pulmonary fibrosis

82
Q

In glycolysis, Fluoride inhibits this enzyme

A

Enolase

83
Q

What is the overall objective of ETC/Oxidative phosphorylation?

A

Oxidize high energy NADH & FADH2

  • Generate electrical potential by passing electrons to oxygen
  • This gradient drives the phosphorylation of ADP to ATP
84
Q

Where is a proton gradient established in ETC?

A

Inner mitochondrial membrane

85
Q

Where does the ETC occur?

A

Inner mitochondrial membrane

86
Q

Describe protein complexes I-IV & their respective prosthetic groups.

A

I: NADH dehydrogenase (FMN & FAD)
II: Succinate dehydrogenase (FMN & FAD)
III: Cytochrome reductase (Fe 3+ - heme)
IV: Cytochrome oxidase (Cu 2+ & Fe 3+)

87
Q

Who oxidizes NADH, FADH2?

A

CoQ

88
Q

Who oxidizes CoQ?

A

Cytochrome C at complex III

89
Q

Who is the final acceptor of electrons?

A

Oxygen at complex IV

90
Q

At which complexes are protons pumped into the intermembrane space of mitochondria?

A

I, III, IV

91
Q

What are the components of complex V?

A

F0- channel/pore for H+ into the matrix

F1- enzyme capable of synthesizing ATP from ADP & Pi

92
Q

Under what conditions is ETC active?

A

High: NADH:NAD+
High: ADP:ATP

93
Q

Under what condition is ETC inactive?

A

Hypoxia

* Tissues are dependent on aerobic metabolism (particularly brain, heart)

94
Q

The following inhibit what in the ETC?

  • Rotenone
  • Piericidin A
  • Amytal
A

NADH dehydrogenase

  • Rotenone - insecticide
  • Piericidin A - antibiotic
  • Amytal - barbituate
95
Q

The following inhibit what in the ETC?

-Antimycin A

A 
Complex III (cytochrome b of cytochrome reductase)
- Antimycin - antibiotic
96
Q

The following inhibit what in the ETC?

-Oligomycin

A 
ATP Synthase (complex V)
- Oligomycin - streptomyces antibiotic
97
Q

The following inhibit what in the ETC?

  • CO
  • Azide
  • H2S
  • CN
A

Cytochrome oxidase (complex IV)

98
Q

Effect of these two inhibitors of ETC is similar to what:

  1. Atractyloside
  2. Bongkrekic acid
A

Oligomycin

  1. toxic from plant - binds intermembrane space portion of adenine nucleotide transporter
  2. from contaminated coconuts - binds matrix portion of adenine nucleotide transporter
99
Q

Differentiate between ETC inhibitors and decouplers with respect to ATP synthesis, ETC activity and O2 consumption.

A

Inhibitors – everything decreases

Decouplers – ETC & O2 consumption increases (ATP syn decreases)

100
Q

What are the effects of DNP, ASA, thermogenin & ionophores on ETC?

A

Destroy the proton gradient (these are uncouplers)

101
Q

Dissipation of the proton gradient generates heat. This uncoupler’s chief role is heat generation. What is it and where is it found?

A

Thermogenin (brown fat - neck & upper back – think newborns!)

102
Q

What is another name for thermogenin and how is it activated?

A

UCP - uncoupling protein

* Activated w/ hormones which release FA’s from triglycerides in brown fat

103
Q

What are uncouplers?

A

Compounds that increase the permeability of the inner mitochondrial membranr

104
Q

What is gluconeogenesis?

A

Making glucose from non-carbohydrates and releasing it into the blood.

105
Q

Where does glucneogenesis take place?

A

90% liver, 10% kidney (overnight fast)

106
Q

Where does gluconeogenesis normally take place during a prolonged fast?

A

60% liver, 40% kidney

107
Q

What stimulates gluconeogenesis?

A

Glucagon & cortisol

108
Q

Why do we need gluconeogenesis?

A

Liver stores of glycogen can only take us so far

- Brain, RBC’s & renal medulla use a lot of ATP, and thus need glucose

109
Q

Describe the “reversal of glycolysis”

A

Pyruvate –> oxaloacetate (malate-oxaloacetate) –> PEP

  1. Pyruvate carboxylase – requires biotin, acetyl coA and CO2 & ATP
  2. PEP carboxylase – requires 1 GTP

F-1,6 biphosphate –> F,6,phosphate (F-1,6, biphosphatase)

G-6-P –> glucose (glucose 6 phosphatase)

110
Q

How is acetyl coA alternatively formed?

A

Beta-oxidation of fatty acids

111
Q

What are substrates for gluconeogenesis?

A

Lactate (muscle + RBC), alanine, glutamine (protein degradation / urea), glycerol (fat),

112
Q

What is the relationship between oxaloacetate and malate?

A

Oxo can’t leave the mitochondria; it is converted into malate, which enters the cytosol and is then re-converted to oxo

113
Q

What will inhibit F-1,6 biphosphatase?

A

High AMP in the liver (this is bad!), will cause the liver to reserve energy for important processes

114
Q

What inactivates pyruvate kinase?

A

Protein kinase A

115
Q

High levels of acetyl coA will stimulate what and inhibit what?

A

Inhibit PDH

Stimulate pyruvate carboxylase

Term 1 (10 decks)

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