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1.2.4. Metabolism, Endocrinology, Haematology > Alcohol Metabolism & Oxidative Stress > Flashcards

Alcohol Metabolism & Oxidative Stress Flashcards

1
Q

Describe how alcohol is metabolised

A

90% met in liver:

1) alcohol is oxidised by alcohol dehydrogenase to acetaldehyde (NAD+ –> NADH)
2) then to acetate by aldehyde dehydrogenase (NAD+ –> NADH),
3) acetate is then converted to acetyl-CoA,
4) used in the TCA cycle or for fatty acid synthesis

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2
Q

What is the recommended alcohol limit for men and women?

A

14 units over 3 days

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3
Q

What part of alcohol met is toxic and causes hangovers?

A

Acetaldehyde – accumulation causes hangovers

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4
Q

Explain how alcohol can cause liver damage

A

Acetaldehyde toxicity normally kept to a minimum by aldehyde dehydrogenase

prolonged excessive alcohol consumption can = acetaldehyde accumulation = liver damage.

Increase in Acetyl-CoA = increased synthesis of fatty acids = fatty liver

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5
Q

Explain the metabolic response to chronic alcohol consumption

A

Increase in Acetyl-CoA = increased synthesis of fatty acids = fatty liver.

Decrease in NAD+/NADH ratio = low NAD+ for conversion of lactate to pyruvate = lactic acidosis, lactate effects kidneys ability to excrete uric acid = gout.

Low NAD+ = low gluconeogenesis = hypoglycaemia

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6
Q

Explain the mechanism of action of Disulfiram

A

Inhibits aldehyde dehydrogenase = accum of acetaldehyde = severe hangover = deterrent

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7
Q

What is oxidative stress?

A

Unbalance between cell damage by ROS/RNS and cell defences = antioxidants, glutathions, superoxide dismutase

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8
Q

What is a free radical?

A

Atom/molecules that contain unpaired electrons = extremely reactive = want to grab electron from somewhere else = propagating reaction

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9
Q

How are superoxide radicals produced

A

In ETC e- can accidently escape chain and react with dissolved O2 = superoxide

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10
Q

What is a reactive oxygen species (ROS)

A

Group of oxygen related compounds that have free radicals = superoxide, hydroxyl radical

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11
Q

What is a reactive nitrogen species (RNS)

A

Group of nitrogen related compounds that have free radicals = nitric oxide

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12
Q

What is the most damaging free radical?

A

Hydroxyl radical = reacts with anything

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13
Q

What are the 2 main types of DNA damage by ROS?

A

Reacting with base = mispairing/mutation.

Reacting with sugar = strand break

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14
Q

How do ROS damage proteins?

A

Backbone damage = fragmentation = degradation.

Sidechain damage = structure change = function change = loss/gain.

Inappropriate disulphide bond formation if ROS take e- from cysteines

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15
Q

How do ROS damage lipids?

A

Damage the cell membrane = propagated chain reaction = membrane integrity fails

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16
Q

What are the sources of biological oxidants?

A

Endogenous = ETC, nitic oxide synthesis, NADPH oxidases.

Exogenous = radiation, drugs, toxins

17
Q

What is the respiratory burst?

A

Phagocytic cells prod superoxide = rapid release = destroy invading bacteria

18
Q

What happens when the respiratory burst is dysfunctional?

A

Chronic granulomatous disease = defect in NADPH oxidase = can’t form ROS to kill bacteria = more prone to infections

19
Q

Outline defences against reactive oxygen species

A

Superoxide dismutase (SOD) = converts superoxide to H2O2 + O2 THEN catalase converts H2O2 to water + oxygen.

Free radical scavengers = vit E = donate H atom to free radicals, nonenzymatic, Vit C regenerates vit E

Glutathione

20
Q

How does glutathione protect the cell against oxidative damage?

A

Glutathione = donates e- to free radical (requires glutathione peroxidase),

regeneration of glutathione requires glutathione reductase (needs NADPH from the pentose phosphate pathway)

21
Q

Explain the role of oxidative stress in galactosaemia

A

Galactosaemia = def in any of the 3 key enzymes

pathway converts = galactose (via NADPH –> NADP+) to galactitol

= using up NADPH which is required to regenerate glutathione which protects cells from free radicals

= prone to ROS damage = crystalline denatured = cataract

22
Q

Explain the role of oxidative stress in the formation of Heinz bodies

A

G6PDH def = low NADPH regeneration = low glutathione regenerated = low protection from free radicals = protein damage = aggregates of cross-lined Hb = Heinz bodies

23
Q

How does a paracetamol overdose cause toxicity to the liver?

A

Overdose = prod of NAPQI toxic metabolite = oxidative damage to liver.

Liver try to combat by reacting NAPQI with glutathione = depletes stores = damage elsewhere

24
Q

What drug should be given after a paracetamol overdose and why?

A

Acetylcysteine = replenishes glutathione levels

25
Q

With a def of galactokinase what substance would build up?

A

Galactitol = build up in osmotic pressure = cataract

26
Q

Does aldehyde dehydrogenase have a low or high Km for acetaldehyde?

A

Low Km

27
Q

Disulphide bone in a protein can form between 2 residues of which AA?

A

Cysteine

28
Q

Which enzyme converts superoxide to H2O2 and oxygen?

A

Superoxide dismutase (SOD)

29
Q

Which enzyme converts H2O2 to water and oxygen?

A

Catalase

30
Q

Which fat soluble vit acts as a free radical scavenger?

A

E

31
Q

What toxic metabolite accumulates in the liver a during paracetamol overdose?

A

NAPQI

32
Q

What is the role of G6PDH?

A

To convert NADP back to NADPH

33
Q

What is the role of NADPH?

A

Reduction of oxidised glutathione = to protect cells

34
Q

What happens in G6PDH def?

A

= limits amount of NADPH prod = reduced amount of glutathione regenerated by NADPH = less protection from oxidative stress

35
Q

What is the clinical sign of G6PDH?

A

Heinz bodies

36
Q

How does NAPQI cause liver damage?

A

Damage to protein/DNA

Oxidative degradation of lipids

1.2.4. Metabolism, Endocrinology, Haematology (21 decks)

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