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2 MEH > 1 Alcohol Metabolism & Oxidative Stress > Flashcards

1 Alcohol Metabolism & Oxidative Stress Flashcards

1
Q

Where does alcohol metabolism occur?

A
  • Liver >90%
  • Remainder is excreted passively in urine and on breath
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2
Q

What are the recommended limits for alcohol consumption?

A

14 units/week spread over at least 3 days for both men & women

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3
Q

Briefly describe the pathway involved in alcohol metabolism

A
  • 1) Alcohol–>Acetaldehyde
    • ​1) Alcohol dehydrogenase
  • 2)Acetaldehyde–>Acetate
    • 2) Aldehyde dehydrogenase
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4
Q

What happens when acetaldehyde accumulates?

A
  • Acetaldehyde is a toxic metabolite
  • Accumulation causes a “Hangover”
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5
Q

What happens to the acetate produced in alcohol metabolism?

A
  • Acetate is conjugated to coenzyme A to form acetyl-CoA
  • Acetyl-CoA:
  1. metabolised in TCA cycle
  2. utilised for fatty acid synthesis
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6
Q

How is acetaldehyde toxicity controlled?

A

Acetaldehyde toxicity normally kept to a minimum by aldehyde dehydrogenase (low Km for acetaldehyde)

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7
Q

How does liver damage occur?

A

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

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8
Q

Identify three forms of liver damage resulting from prolonged and excessive alcohol consumption

A
  • “Fatty liver”
  • Alcoholic hepatitis
  • Alcoholic cirrhosis
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9
Q

Indicate how liver damage can lead to changes in liver metabolism

A
  • Excess NADH (decreased NAD:NADH)
  • Excess Acetyl-CoA
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10
Q

What are the systemic consequences of liver damage due to prolonged and excessive alcohol consumption? (3)

A
  • Lactic acidosis
  • Hypoglycaemia
  • Gout
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11
Q

Illustrate how excess NADH and Acetyl-CoA resulting from alcoholic liver damage can lead to the following consequences:

  • Lactic acidosis
  • Gout
  • Hypoglycaemia
  • Fatty liver
A
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12
Q

Which drug can be used to treat chronic alcohol dependence?

A

Disulfiram

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13
Q

What is oxidative stress?

A

Disturbance in the balance between the production of reactive oxygen species (free radicals) and antioxidant defenses

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14
Q

What is a free radical?

A

A free radical is an atom or molecule that contains 1/more unpaired electrons and is capable of independent existence e.g. OH•

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15
Q

Why are free radicals so damaging?

A
  • Free radicals are usually very reactive and tend to acquire electrons from other atoms, molecules or ions
  • Reaction of a radical with a molecule typically generates a second radical thereby propagating damage
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16
Q

What are the two types of free radicals found in the body?

A
  • Reactive Oxygen Species eg. Super oxide, Hydrogen peroxide
  • Reactive Nitrogen Species eg. Nitric oxide, Peroxynitrate
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17
Q

Which three structures can ROS damage?

A
  • DNA
  • Proteins
  • Lipids
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18
Q

Outline the two ways in which ROS can damage DNA

A
  • ROS reacts with base – mispairing
  • ROS reacts with sugar (ribose or deoxyribose) – strand break
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19
Q

What are the possible consequences of ROS damage to DNA?

A
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20
Q

Outline the two ways that ROS can damage proteins and the consequences of this.

A

If ROS takes electrons from cysteine- cause misfolding/crosslinking

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21
Q

Disulphide bonds are formed between thiol groups of cysteine residues and play an important role in folding and stability of some proteins.

What happens when ROS interfere with these bonds?

A

Inappropriate disulphide bond formation can occur if ROS takes electrons from cysteines causing misfolding, crosslinking and disruption of function e.g. enzyme

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22
Q

Which process in triggered when ROS react with lipids?

A

Lipid peroxidation

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23
Q

In three steps, describe how lipid peroxidation occurs

A

⇒ Free radical extracts H+ from a polyunsaturated fatty acid in membrane lipid

⇒ Lipid radical forms & reacts with O2 to form a lipid peroxyl radical

⇒ Chain reaction formed as lipid peroxyl radical extracts hydrogen from nearby fatty acid

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24
Q

What are the consequences of lipid peroxidation? (think membrane)

A

Hydrophobic environment of bilayer disrupted and membrane integrity fails

25
Q

Identify three endogenous sources of biological oxidants

A
  • Electron transport chain (electrons accidently escape chain)
  • Nitric oxide synthases
  • NADPH oxidases
26
Q

Identify four exogenous sources of biological oxidants

A
  • Radiation- UV light, x-rays
  • Pollutants
  • Drugs (eg primaquine- anti-malarial)
  • Toxins (eg herbicide)
27
Q

Explain how the ETC can be an endogenous source of ROS

A
  • Electrons pass through ETC and reduce oxygen to form H2O at Complex IV
  • Occasionally electrons can accidently escape chain and react with dissolved O2 to form superoxide
28
Q

Explain the pathway in which nitric oxide synthase acts as an endogenous source of ROS

A

Arginine → Citrulline + NO•

  • Nitric oxide synthase catalyses this reaction
  • NO• is toxic in high levels
29
Q

What are the three types nitric oxide synthase?

A
  • iNOS: inducible nitric oxide synthase (direct toxic effect in phagocytes)
  • eNOS: endothelial nitric oxide synthase (signalling)
  • nNOS: neuronal nitric oxide sytnthase (signalling)
30
Q

Illustrate how biological oxidants are part of antimicrobial defence system

A
  • Rapid release of superoxide & H2O2 from phagocytic cells
  • ROS and peroxynitrite destroy invading bacteria

=Respiratory Burst

31
Q

What is chronic granulomatous disease?

A

Genetic defect in NADPH oxidase complex

Enhanced susceptibility to bacterial infections e.g. pneumonia, cellulitis, impetigo, absesses

32
Q

Identify three cellular defences against biological oxidants

A
    • Superoxide dismutase
    • Catalase
    • Glutathione
33
Q

Explain the action of superoxide dismustase as a cellular defence

A
  • Converts superoxide to hydrogen peroxide and oxygen
  • Primary defence as superoxide is strong initiator of chain reactions
34
Q

Explain the action of catalase as a cellular defence

A
  • Converts hydrogen peroxide to water and oxygen
  • Important in immune cells to protect against oxidative burst
35
Q

What is glutathione?

A

Glutathione is a tripeptide synthesised by body to protects against oxidative damage

36
Q

Explain the action of glutathione as a cellular defence

A
  1. ⇒ The thiol group of Cys donates e− to ROS
  2. ⇒ GSH then reacts with another GSH to form a disulphide (GSSG)
  3. –> Glutathione reductase:
    1. Reduces GSSG–> GSH
    2. Catalyses the transfer of electrons from NADPH to disulphide bond
37
Q

Identify the two requirements necessary for the action of glutathione.

A
  • Glutathione peroxidase requires selenium
  • NADPH from the pentose phosphate pathway
38
Q

Which vitamins act as free radical scavengers?

A
  • Vitamin C
  • Vitamin E
39
Q

How do free radical scavengers act as cellular defences against biological oxidants?

A

Reduce free radical damage by donating hydrogen atom (and its electron) to free radicals in a nonenzymatic reaction

40
Q

Explain and illustrate how Vitamin C and E act as free radical scavengers

A
  • Vitamin E: lipid soluble antioxidant important for protection against lipid peroxidation
  • Vitamin C: water soluble antioxidant important in regenerating the reduced form of Vitamin E
41
Q

Identify 5 symptoms of galactosaemia. (6)

A
  • Hepatomegaly & cirrhosis
  • Renal failure
  • Vomiting
  • Seizure & brain damage
  • Cataracts
  • Hypoglycaemia
42
Q

In galactosaemia, the accumulation of galactose can lead to the formation of cataracts.

In four steps, describe how this occurs

A
  1. ⇒ Increased activity of aldose reductase consumes excess NADPH
  2. ⇒ Compromised defences against ROS damage
  3. ⇒ Crystallin protein in lens of eye denatured (+ osmotic pressure)
  4. ⇒ Cataracts form
43
Q

In 5 steps, explain the consequences of GSPDH deficiency

A

⇒ Decreased G6PDH activity limits amount of NADPH

⇒ Less NADPH available for reduction of GSSG back to GSH

⇒ Lower GSH = less protection against oxidative stress

⇒ Lipid peroxidation & protein damage

⇒ Haemolysis

44
Q

What are heinz bodies?

A
  • Heinz bodies are aggregates of cross-linked haemoglobin
  • The precipitated haemoglobin stains dark within RBCs
45
Q

What are the effects of heinz bodies?

A
  • Bind to cell membrane altering rigidity
  • Increased mechanical stress when cells squeeze through small capillaries
  • Spleen removes bound Heinz bodies resulting in “blister cells”
46
Q

How much energy does alcohol contain?

A

29kJ/g

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47
Q

What conditions can be cause by prolonged and excessive alcohol consumption and why? (3)

A
  1. ‘Fatty liver’
  2. Alcohol hepatitis
  3. Alcohol Cirrhosis (scar tissue formation)

Due to increase levels:

  • NADH
  • Acetyl-CoA
48
Q

How can chronic alchohol consumption cause gout?

A
  • Lactate accumulates in blood
  • Kidney’s inability to excrete uric acid reduced
  • Urate crystals accumulate in tissues=gout
49
Q

How can chronic alcohol consumption cause hypoglycaemia?

A
  • Inadequate NAD+ for glycerol metabolism
  • Inadequate NAD+ for conversion of lactate–>pyruvate
  • Gluconeogenesis deficit
50
Q

How can chronic alcohol consumption cause a ‘fatty liver’?

A
  • Decrease NAD+/NADH ratio
  • Inadequate NAD+ for fatty acid oxidation
  • Increased acetyl-CoA- increased synthesis of fatty acids and ketone bodies- increased Triacylglycerol synthesis
51
Q

What is disulfiram used to treat and how does it work?

A

Chronic Alcohol dependence

Inhibits aldehyde dehydrogenase

Acetaldehyde accumulates- symptoms of hangover

52
Q

Name some diseases which can be caused by oxidative stress.

A
  1. Cancer
  2. MS
  3. CVS disease
  4. Rheumatoid arthiritis
  5. Crohn’s disease
  6. COPD
  7. Alzheimer’s
53
Q

What is Nitric Oxide used for in the body?

A

Signalling (Vasoldilation, neurotransmission)

54
Q

What is galactosaemia?

A

Deficiency in any 3 enzymes favouring conversion of galactose–> galactitol

55
Q

What are heinz bodies a clinical sign of?

A

G6PDH deficiency

56
Q

What are the symptoms of a G6PDH deficiency?

A
  1. Anaemia
    1. HB conc decreased
    2. Increased reticulocytes
  2. Jaundice
    1. By-product of RBC breakdown
57
Q

How is Paracetamol safely metabolised (usually)?

A

Conjugation with:

  • glucuronide
  • sulphate
58
Q

What happens (metabolically) in a paracetamol overdose?

A

NAPQI toxis metbolite- accumulates:

  • Oxidative damage- liver cell
  • Glutathione depletion
59
Q

What antidote is used for a paracetamol overdose and how does it work?

A

Acetylcysteine- replenish Glutathione levels

2 MEH (18 decks)

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