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Semester 2-MEH > Session 3-Alcohol Metabolism And Oxidative Stress > Flashcards

Session 3-Alcohol Metabolism And Oxidative Stress Flashcards

1
Q

Where is most alcohol metabolised?

A

Liver

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2
Q

Complete the sentence:

Alcohol is oxidised by _________ ________________ to acetaldehyde and then to _________ by ______________ ________________.

A

Alcohol dehydrogenase
Acetate
Aldehyde dehydrogenase

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3
Q

What is acetate converted to and where is this product used?

A

Acetyl-CoA

Used in TCA cycle or for fatty acid synthesis

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4
Q

Which enzymes can oxidise smaller amounts of alcohol?

A

Cytochrome P450 2E1 (CYP2E1)

Catalase in the brain

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5
Q

What does the accumulation of acetaldehyde cause?

A

“Hangover”

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6
Q

How is acetaldehyde toxicity kept to a minimum?

A

Aldehyde dehydrogenase

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7
Q

True or false: aldehyde dehydrogenase has a high Km for acetaldehyde

A

FALSE - low Km

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8
Q

How can alcohol consumption lead to liver damage?

A

Prolonged and excessive consumption can cause sufficient acetaldehyde accumulation to cause liver damage

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9
Q

What leads to changes in liver metabolism?

A

Excess of NADH and acetyl-CoA

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10
Q

How can alcohol oxidation lead to lactic acidosis?

A

Decrease in NAD+/NADH ratio -> inadequate NAD+ for conversion of lactate to pyruvate -> lactate accumulates in blood -> lactic acidosis

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11
Q

How does alcohol oxidation lead to urate crystals accumulating in tissues, producing gout?

A

Decrease in NAD+/NADH ratio -> inadequate NAD+ for conversion of lactate to pyruvate -> lactate accumulates in blood -> kidney’s ability to excrete uric acid reduced -> gout

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12
Q

How does alcohol oxidation lead to hypoglycaemia?

A

Decrease in NAD+/NADH ratio -> inadequate NAD+ for glycerol metabolism -> deficit in gluconeogenesis -> hypoglycaemia

OR

Decrease in NAD+/NADH ratio -> inadequate NAD+ for conversion of lactate to pyruvate -> deficit in gluconeogenesis -> hypoglycaemia

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13
Q

How does alcohol oxidation lead to fatty liver?

A

Increased acetyl-CoA -> increased synthesis of fatty acids and ketone bodies ->increased synthesis of triacylglycerol -> fatty liver

OR

Lower lipoprotein synthesis -> fatty liver

OR

Decrease in NAD+/NADH ratio -> inadequate NAD+ for fatty acid oxidation -> increased synthesis of triacylglycerol -> fatty liver

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14
Q

What is used as an adjunct in the treatment of chronic alcohol dependence?

A

Disulfiram

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15
Q

What is disulfiram an inhibitor of?

A

Aldehyde dehydrogenase

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16
Q

What causes a ‘hangover’ in patients who drink alcohol?

A

Acetaldehyde accumulation

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17
Q

What are the two species of free radicals?

A

1) reactive oxygen species

2) reactive nitrogen species

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18
Q

What does the reaction between superoxide and nitric oxide form?

A

Peroxynitrite

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19
Q

What is the formula of peroxynitrite?

A

ONOO-

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20
Q

True or false: peroxynitrite is a free radical

A

FALSE - but it is a powerful oxidant that can damage cells

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21
Q

Molecular oxygen is a biradical. What does this mean?

A

It has two unpaired electrons in different orbitals

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22
Q

How is superoxide formed?

A

Adding electron to molecular oxygen

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23
Q

True or false: hydrogen peroxide is not a free radical

A

TRUE - can react (eg with Fe2+) to produce free radicals

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24
Q

What is the most reactive and damaging free radical?

A

Hydroxyl

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25
Q

What are the two main types of reactive oxygen species (ROS) damage to DNA?

A

1) ROS reacts with base-can lead to mispairing and mutation

2) ROS reacts with sugar (ribose or deoxyribose)-can cause strand break and mutation on repair

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26
Q

How can reactive oxygen species lead to cancer?

A

ROS reacts with DNA -> DNA damage -> failure in repair can lead to mutation -> cancer

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27
Q

What can be used as a measurement of oxidative damage in cells?

A

Amount of 8-oxo-dG

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28
Q

How can reactive oxygen species lead to protein degradation?

A

Fragmentation of backbone -> protein degradation

OR

Modified AA side chain -> change in protein structure -> protein degradation

29
Q

How can reactive oxygen species lead to loss or gain of function of proteins?

A

Modified AA side chains -> change in protein structure -> loss/gain of function

30
Q

What do disulphide bonds play an important role in?

A

Folding and stability of some proteins (secreted proteins or in extracellular domains of membrane proteins)

31
Q

Where do disulphide bonds form between?

A

Thiol groups of cysteine residues

32
Q

When can inappropriate disulphide bond formation occur and what can this cause?

A

If reactive oxygen species take electrons from cysteines, causing misfolding, crosslinking and disruption of function

33
Q

How can reactive oxygen species damage lipids?

A

1) Free radical extracts hydrogen atom from a polyunsaturated fatty acid in membrane lipid
2) Lipid radical formed which can react with oxygen to form lipid peroxyl radical
3) Chain reaction formed
4) Hydrophobic environment of bilayer disrupted and membrane integrity falls

34
Q

What are some endogenous sources of biological oxidants?

A
  • electron transport chain
  • nitric oxide synthases
  • NADPH oxidases
35
Q

What are some exogenous sources of biological oxidants?

A
  • radiation
  • pollutants
  • drugs
  • toxins
36
Q

How can the electron transport chain lead to the production of reactive oxygen species?

A

1) NADH and FADH2 supply electrons
2) electrons pass through ETC and reduce oxygen to form water at complex IV
3) occasionally electrons can escape chain and react with dissolved oxygen to form superoxide

37
Q

What are the three types of nitric oxide synthase (NOS)?

A

1) iNOS - inducible nitric oxide synthase
2) eNOS - endothelial nitric oxide synthase
3) nNOS - neuronal nitric oxide synthase

38
Q

What do the three types of nitric oxide synthases do?

A

1) iNOS produces high NO concentrations in phagocytes for direct toxic effect
2) eNOS for signalling
3) nNOS for signalling

39
Q

What does nitric oxide synthase convert arginine into?

A

Citrulline

40
Q

What happens when citrulline reacts with nitric oxide?

A

1) toxic effects at high level

2) signalling molecule for vasodilation and neurotransmission

41
Q

What is a respiratory burst?

A

1) Rapid release of superoxide and hydrogen peroxide from phagocytic cells
2) Reactive oxygen species and peroxynitrite destroy invading bacteria

42
Q

What is chronic granulomatous disease?

A

Genetic defect in NADPH oxidase complex, causing enhanced susceptibility to bacterial infections such as:

  • pneumonia
  • abscesses
  • impetigo
  • cellulitis
43
Q

Which enzyme converts superoxide to hydrogen peroxide and oxygen?

A

Superoxide dismutase

44
Q

What are the three isoenzymes of superoxide dismutase?

A

1) Cu+ Zn2+ cytosolic
2) Cu+ Zn2+ extracellular
3) Mn2+ mitochondria

45
Q

What does catalase convert hydrogen peroxide into?

A

Water and oxygen

46
Q

What does catalase protect against?

A

Oxidative burst

47
Q

How can catalase lead to grey hair?

A

Declining levels of the enzyme in hair follicles with age explains grey hair because the hair bleaches itself (H2O2)

48
Q

What is the reduced form of glutathione?

A

GSH

49
Q

What is the oxidised form of glutathione and how does it form?

A

Disulphide (GSSG)

Thiol group of Cys donates electron to ROS and GSH reacts with another GSH to form GSSG

50
Q

Which element does glutathione peroxidase require?

A

Selenium (facilitates the transfer of electrons)

51
Q

Which enzyme reduced GSSG back to GSH?

A

Glutathione reductase - catalyses transfer of electrons from NADPH to disulphide bond

52
Q

True or false: NADPH from pentose phosphate pathway is essential for protection against free radical damage

A

TRUE

53
Q

Which vitamins are free radical scavengers?

A

E

C (ascorbic acid)

54
Q

What kind of antioxidant is vitamin E and what is it important for?

A

Lipid soluble

Important for protection of lipid bilayer against lipid peroxidation

55
Q

What kind of antioxidant is vitamin C and what is it important for?

A

Water soluble

Important role in regenerating reduced form of vitamin E

56
Q

How do free radical scavengers reduce free radical damage?

A

Donate hydrogen atom and its electron to free radicals in a nonenzymatic reaction

57
Q

What are some other examples of free radical scavengers?

A
  • carotenoids
  • uric acid
  • flavonoids
  • melatonin
58
Q

What is oxidative stress?

A

Oxidants > defences

59
Q

How can glucose-6-phosphate deficiency lead to haemolysis?

A

Limits amount of NADPH -> lower GSH -> less protection against oxidative stress -> oxidative stress -> lipid peroxidation and protein damage -> haemolysis

60
Q

What are Heinz bodies?

A

Dark staining within RBCs resulting from precipitated Hb

61
Q

What do Heinz bodies do?

A

Bind to cell membrane, altering rigidity

Increased mechanical stress when cells squeeze through small capillaries

62
Q

Which organ removes bound Heinz bodies and what does this result in?

A

Spleen

Blister cells

63
Q

What are Heinz bodies a clinical sign of?

A

Glucose-6-phosphate dehydrogenase deficiency

64
Q

Where does the metabolism of paracetamol occur?

A

Hepatocyte

65
Q

At a prescribed dosage, paracetamol can be safely metabolised by conjunction with which two substances?

A

1) glucuronide

2) sulphate

66
Q

What does a high level of paracetamol lead to the accumulation of?

A

Toxic metabolite NAPQI

67
Q

Describe the oxidative damage to liver cell caused by NAPQI

A
  • lipid peroxidation
  • damage to proteins
  • damage to DNA
68
Q

What is the antidote for increased levels of paracetamol?

A

Acetylcysteine - replenishes glutathione levels

Semester 2-MEH (21 decks)

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