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MEH Revision > 1 - Oxidative Stress and Alcohol Metabolism > Flashcards

1 - Oxidative Stress and Alcohol Metabolism Flashcards

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1
Q

Put the following in order or energy content per gram:

  • Alcohol
  • Protein
  • Fat
  • Carbohydrate
A
  • Fat
  • Alcohol
  • Protein/Carbohydrate
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2
Q

Where is 90% of alcohol metabolised?

Where is the remained metabolised?

A

The Liver

Passively excreted in urine and the breath

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3
Q

Give an overview of how alcohol is metabolised?

A
  • Alcohol is oxidised by alcohol dehydrogenase to acetaldehyde
  • Acetaldehyde converted to acetate by aldehyde dehydrogenase
  • Acetate converted to acetyl-CoA for use in the TCA cycle or fatty acid synthesis
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4
Q

Which cytochrome P450 enzyme can oxidise alcohol?

A

2E1 (CYP2E1)

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5
Q

What enzyme in the brain can oxidise alcohol?

A

Catalase

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6
Q

What is the weekly recommended limit for alcohol consumption?

A

14 units per week over at least 3 days

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7
Q

At what rate is alcohol eliminated by the body?

A

~7g per hour

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8
Q

What type of elimination kinetics does alcohol metabolism show? What does this mean?

A

Zero order kinetics

- Constant rate of metabolism - higher blood alcohol level will not cause the elimination to happen any faster

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9
Q

An intermediate in alcohol metabolism is acetaldehyde. What effects does this have on the body?

A
  • Toxic metabolite

- Accumulation causes hangover (along with dehydration - ADH inhibition) and cirrhosis in the long-term

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10
Q

What molecule is reduced in both conversion of:

  • alcohol to acetaldehyde?
  • acetaldehyde to acetate?
A

NAD+ converted to NADH (NAD+ reduced)

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11
Q

Why is aldehyde dehydrogenase very effective in keeping acetaldehyde toxicity to a minimal level?

A

Very low Km for acetaldehyde (high affinity)

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12
Q

During ……….. and ……….. alcohol consumption, sufficient acetaldehyde accumulates to cause liver damage

A

Prolonged and excessive

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13
Q

What causes fatty liver to occur due to alcohol consumption?

A
  • Increased acetyl-CoA produced
  • Increased synthesis of fatty acids and ketone bodies (also less NAD+ available for B-oxidation of fatty acids)
  • Increased synthesis of triacylglycerols results in fatty deposits in the liver
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14
Q

What causes hypoglycaemia in chronic alcohol consumption?

A
  • Decrease in NAD+/NADH ratio
  • Inadequate NAD+ for conversion of lactate to pyruvate or for glycerol metabolism
  • Less gluconeogenesis in the liver = hypoglycaemia
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15
Q

What causes gout in chronic alcohol consumption?

A
  • Decrease in NAD+/NADH ratio
  • Inadequate NAD+ for conversion of lactate to pyruvate
  • Lactate accumulates in the blood
  • Kidney can’t secrete as much uric acid
  • Urate crystals accumulate in the tissues
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16
Q

What causes lactic acidosis in chronic alcohol consumption?

A
  • Decrease in NAD+/NADH ratio
  • Inadequate NAD+ for conversion of lactate to pyruvate
  • Lactate accumulates in the blood
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17
Q

What is Disulfiram? What does it do?

A
  • Drug used for treatment of chronic alcohol dependence
  • Inhibits aldehyde dehydrogenase
  • If patients drinks alcohol, acetaldehyde accumulates causing an intense ‘hangover’ - classical conditioning to feel sick at the sight of alcohol
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18
Q

Oxidative stress is a balance between cell ……………. (ROS and RNS) and cell ……………… (antioxidants)

A

Damage

Defences

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19
Q

What conditions are commonly related to oxidative stress?

A
  • Alzheimer’s disease
  • Reumatoid arthritis
  • Crohn’s disease
  • COPD
  • Ischaemia/reperfusion injury
  • Cancer
  • Pancreatitis
  • Parkinson’s disease
  • Multiple sclerosis
  • Cardiovascular disease
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20
Q

What is a free radical?

A
  • An atom or molecule with one or more unpaired electrons that is capable of independent existence
  • Very reactive and tend to propagate damage to other molecules
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21
Q

What are the three main reactive oxygen species (ROS)?

Which of these are free radicals?

A
  • Superoxide (O2.-)
  • Hydrogen peroxide (H2O2)
  • Hydroxyl (OH.)

Superoxide and hydroxyl are free radicals. Hydrogen peroxide is a highly reactive, diffusible and toxic molecule.

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22
Q

What ROS radical is the most damaging?

Study These Flashcards
A

Hydroxyl radical (OH.)

  • Reacts strongly with anything
23
Q

What are the two type of reactive nitrogen species (RON)?

Study These Flashcards
A
  • Nitric oxide (NO.)

- Peroxynitrite (ONOO-)

24
Q

How is peroxynitrite formed?

Study These Flashcards
A

Superoxide reacts with nitric oxide

25
What are two ways in which ROS can damage DNA?
- ROS reacts with base (mispairing and mutation) | - ROS reacts with sugar (strand break and mutation on repair)
26
The presence of what molecule in DNA is used as a measurement of oxidative damage?
- 8-oxo-deoxyguanosine | - Formed from deoxyguanosine by ROS and accumulates in DNA
27
What are the two main pathways that ROS can damage proteins?
- ROS fragments protein backbone - ROS modifies the amino acids (e.g. carbonyls, hydroxylation, dimerisation, disulphide bonds) Both lead to loss-of-function and degradation
28
In which level of protein structure do disulphide bonds form?
Tertiary structure
29
How do disulphide bonds form?
- bridges formed between thiol groups (-SH) of cysteine residues
30
How can ROS damage lipids?
- Free radicals remove hydrogen from fatty acid chain in lipid membranes forming a lipid radical - Reacts with oxygen to for a lipid peroxyl radical - Chain reaction with other nearby fatty acids disrupts the lipid membrane
31
Give some endogenous sources of oxidants?
- Electron transport chain - Peroxidases - Nitric oxide synthases - Lipooxygenases - NADPH oxidases - Xanthine oxidase - Monoamine oxidase
32
Give some exogenous sources of oxidants?
- Radiation - cosmic rays, UV, X-rays - Pollutants - Drugs - Primaquine (anti-malarial) - Toxins - Paraquat (herbicide)
33
How does the electron transport chain operate as a source of endogenous free radicals?
- NADH and FAD2H supply e- - e- passes through the ETC and reduces oxygen - Some electrons escape the chain and react with O2 to form superoxide
34
Describe the action of nitric oxide synthase (NOS).
- Arginine is converted to citrulline and nitric oxide by NOS
35
What are the three types of nitric oxide synthase (NOS)?
- iNOS - inducible - high NO concentrations for toxic effects in phagocytes - eNOS - endothelial - signalling in vessels - nNOS - neuronal - signalling in neurones
36
Give some functions of nitric oxide.
Signalling: - Vasodilation - Neurotransmission - S-nitrosylation Part of the respiratory burst in phagocytes
37
What is released in the respiratory burst and what does it do?
- Rapid release of superoxide, H2O2 and peroxynitrite from phagocytic cells (e.g. neutrophils and monocytes) - Destroy invading bacteria
38
What is chronic granulomatous disease?
- Genetic defect in NADPH oxidase complex of respiratory burst - Enhanced susceptibility to bacterial infections (e.g. pneumonia, cellulitis, impetigo)
39
What are the actions of superoxide dismutase and catalase in cellular defence?
- Superoxide dismutase converts superoxide to H2O2 | - Catalase converts H2O2 to water and oxygen
40
What is glutathione and what does it do?
- Tripeptide synthesised by the body - Protects against oxidative damage - Reduced form (GSH) and oxidised form (GSSG)
41
How does glutathione protect against oxidative damage?
- Glutathione is oxidised by glutathione peroxidase - e- from GSH reacts with H2O2 to form water - Two oxidised GSH molecules for a disulphide bridge - forms GSSG (reduced back to GSH by glutathione reductase)
42
Why is NADPH essential to action of glutathione?
- Electrons from NADPH required for reduction of GSSG back to GSH by glutathione reductase - NADPH from pentose phosphate pathway is essential
43
Give an overview of the pentose phosphate pathway.
- Starts with glucose-6-phosphate - Source of NADPH and C5-sugars - No ATP synthesised - Rate limited by G6P dehydrogenase
44
Describe the role of vitamin C and vitamin E in defence against free radicals
- Vitamin E - lipid-soluble antioxidant - protects against lipid peroxidation - Vitamin C - water soluble - regenerates reduced form of vitamin E
45
Deficiency in which enzymes can lead to galactosaemia?
- Galactokinase - Uridyltransferase - UDP-galactose epimerase
46
Galactose is converted to galactitol by ......... ................
Aldose reductase
47
How does galactosaemia contribute to the development of cataracts?
- Deficiency of enzymes in galactosaemia favours conversion of galactose into galactitol (increases osmotic pressure in the eye lens) - Increased activity of aldose reductase uses more NADPH = less defence against ROS. The crystallin protein in the eye lens is denatured
48
How does G6PDH deficiency affect GSH?
- A decrease in G6PDH activity limits production of NADPH - NADPH is required for reduction of GSSG back to GSH - Lower GSH = less protection from oxidative stress
49
What are Heinz bodies?
- Aggregates of cross-linked haemoglobin within red blood cells (induced by H2O2) - Bind to the cell membrane altering rigidity, increases effects of mechanical stress on RBCs (haemolysis) - Removed by the spleen
50
Heinz bodies are a clinical sign of what condition?
G6PDH deficiency
51
At prescribed dosage, how is paracetamol metabolised?
- Conjugated with glucuronide or sulphate in the liver
52
With high levels of paracetamol, how are toxic effects exerted?
- Toxic metabolite NAPQI accumulates - NAPQI has direct toxic effects (lipid peroxidation, DNA and protein damage) - Glutathione can remove NAPQI but eventually will become depleted
53
What is the antidote to paracetamol overdose and how does it work?
Acetylcysteine | - Replenishes glutathione levels to breakdown toxic NAPQI

MEH Revision (4 decks)

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