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MEH * > 1.1 Alcohol metabolism and oxidative stress > Flashcards

1.1 Alcohol metabolism and oxidative stress Flashcards

1
Q

Where is alcohol removed from the body?

A

Metabolised by the liver
Catabolised by enzyme in the brain
Remainder excreted passively in urine and on breath

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2
Q

How is alcohol metabolised?

A

In the liver
Alcohol is oxidised by alcohol dehydrogenase (using NAD+ to NADH) into acetaladehyde
Then, acetaldehyde is converted into acetate using aldehyde dehydrogenase (and another NAD+ to NADH)

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3
Q

What causes a hangover?

A

A build up of acetaldehyde - its a toxic metabolite

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4
Q

What can acetate be used for?

A

Can form acetyl- CoA for TCA cycle or fatty acid synthesis

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5
Q

What’s the rate of alcohol metabolism? And what are the recommended units?

A

One unit = 8g
Eliminate alcohol at rate of 7g an hour
Can find one unit in half a pint of beer or a small glass of wine

Recommended units = 14 a week spread over 3 days

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6
Q

What can happen in cases of excess alcohol consumption?

A

Build up of acetaldehyde, not enough aldehyde dehydrogenase to convert it to acetate so get
- liver cirrhosis
- alcohol hepatitis
- ‘fatty liver’
Also, excess NADH and acetyl CoA production lead to changes in liver metabolism.

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7
Q

How can you get a ‘fatty liver?’

A
  • Increased acetyl co A
  • increased synthesis of fatty acid and ketone bodies
  • increased synthesis of triacylglycerol
    (And low lipoprotein synthesis)
    = FATTY liver
    Also, less NAD+ = cant do fatty acid oxidation = more triglycerides form
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8
Q

How can you get lactic acidosis?

A
  • decrease in NAD+/NADH ratio
  • cant convert lactate to pyruvate as not enough NAD+
  • lactate accumulates in blood
    = ACIDOSIS
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9
Q

How can alcoholism cause gout?

A
  • Lower NAD/NADH ratio
  • not enough NAD to convert lactate to pyruvate
  • lactate accumulates in blood
  • kidneys ability to excrete Uric acid reduced
  • urate crystals accumulate = gout
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10
Q

How can alcoholism cause hypoglycaemia?

A
  • decreased NAD/NADH ratio
  • inadequate NAD for glycerol metabolism
  • deficit in gluconeogenesis
    = HYPOGLYCEMIA
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11
Q

What can be used to treat alcohol dependence and how does it work?

A
  • Disulfiram
  • inhibits aldehyde dehydrogenase
  • so if patient drinks, acetylaldehyde will accumulate = get symptoms of a hangover and feel sick. So, will associate drinking with a negative feeling = gets them off it.
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12
Q

ROS and RNS can cause oxidative stress. When does oxidative stress occur?

A

When there is an imbalance of oxidants and defences, with more oxidants than our defences can handle

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13
Q

What’s a free radical?

A

An atom with an unpaired electron.

NB: reaction of a radical with a molecule typically generates a second radical thereby propagating damage

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14
Q

Name a reactive nitrogen species and how it is formed. What can it do?

A
  • Peroxynitrite (ONOO-) is a RNS
  • formed from superoxide and nitric oxide
  • is a powerful oxidant
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15
Q

How is superoxide formed??

A

Add an electron to normal oxygen = superoxide free radical

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16
Q

What’s the most damaging and reactive free radical and ROS?

A

OH* !!!!!!!!!!!!!!

NB: formed from H2O2, which itself is not a free radical but can readily react with things like fe2+ to make free radicals. Gnarly

17
Q

How can ROS cause cancer?

A
  • reacts with dna
  • dna damage
  • failure in repair = mutation
  • can lead to cancer
18
Q

How can ROS damage proteins (backbone and side chains)?

A

Backbone
- fragmentation = protein degradation

Side chains

  • modified amino acids and bonds e.g. disulfied bonds in protein structure = change in protein structure
  • loss of function = protein degradation

Sometimes can have gain of function.

19
Q

What are disulfied bonds formed between?

A

The thiol groups of cysteine residues.

NB: ROS can cause disulfied bonds to form in random places = miss-folding = chaos.

20
Q

How can ROS damage lipids?

A
  • Free radical (OH*) takes hydrogen from polyunsaturated fatty acid in membrane lipid
  • lipid radical formed, can react with oxygen to form lipid peroxyl radical
  • hydrophobic environment of bilayer disrupted and membrane integrity falls (I’m yelling timber)
21
Q

Name 3 endogenous and 3 exogenous sources of biological oxidants.

A

Endogenous

  • electron transport chain (electron escapes and reacts with o2 to form superoxide)
  • NADPH oxidises
  • nitric oxide syntheses

Exogenous

  • radiation
  • pollutants
  • toxins
22
Q

What are the effects of NO*?

A

Signalling molecule

  • vasodilation
  • neurotransmission
  • toxic at high levels
23
Q

What is respiratory burst?

A
  • rapid release of superoxide and h2o2 from phagocytise cells
  • ROS and peroxynitrite destroy invading bacteria
  • part of antimicrobial defence system
24
Q

What is chronic granulomatous disease?

A

Genetic defect in NADPH oxidase complex = increases susceptibility to bacteria infections such as:

  • cellulitis
  • abscesses
  • pneumonia
  • atypical infections
25
Q

What is the role of superoxide dismutase? (SOD)

A
  • converts superoxide to h202 and oxygen

- is cytosolic, extracellular and mitochondrial

26
Q

What is the role of catalase?

A
  • converts h202 to water and oxygen
27
Q

What is glutathione?

A
  • tripeptide synthesised to protect against oxidative damage
  • has cysteine group for disulfied bonds to form
  • also glutathione peroxidase which facilitates this process converts h202 to h20 = reduces amount of free radicals around
28
Q

What is the pentose phosphate pathway?

A
  • starts from glucose 6 phosphate
  • important source of NADPH for processes e.g detoxification and reducing
  • no atp produces, just co2
  • produces C5 sugar ribose for things e.g nucleotides and DNA
  • rate limiting enzyme is glucose 6 phosphate dehydrogenase
29
Q

Name two free radical scavengers and how they work.

A

Vitamin E

  • important for protection against lipid peroxidation
  • turns lipid radical back into normal lipid

Vitamin c
- regenerates reduced form of vitamin E

30
Q

How do people get galactosaemia? And then cataracts?

A

Deficiency in one of three enzymes

  • uridyl transferase
  • galactokinase
  • UDP galactose epimerise

Means that aldosterone reductase will have to work harder to remove galactose and convert galactose (formed from glucose and dietary lactose) into galactitol = increased osmotic pressure in eye = can get cataracts.

NB: increased activity of aldose reductase consumped NADPH = compromised defence against ROS damage - crystalline protein in lens of eye denature = cataracts

31
Q

What are the consequences of a glucose 6 phosphate dehydrogenase reaction?

A
  • decrease in activity = limits amount of NADPH needed for reduction of glutathione in its oxidised form
  • lower reduced glutathione means less protection against oxidative stress
  • as a result can get lipid peroxidatio and protein damage, which may present as Heinz bodies (aggregation of cross linked haemoglobin) (haemolysis)
32
Q

What are Heinz bodies?

A
  • dark staining within red blood cell resulting from precipitated haemoglobin
  • bind to cell membrane altering rigidity
  • increase mechanical stress when squeezing through small capillaries
  • spleen removes them
  • clinical sign of G6PDH deficiency
33
Q

How is paracetamol metabolised?

A
  • at prescribed dosage, is metabolised with sulphate or glucuronide
  • high levels taken = toxic metabolism NAPQI is made. Causes oxidative damage to live cells (proteins, DNA and lipid peroxidation)
  • also converted to glutathione which tries to fix this but then you get glutathione depletion since its working so hard and cant keep up with NAPQIs effects
  • treat with acetyl cysteine to replenish glutathione levels

MEH * (21 decks)

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