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MEH > Alcohol Metabolim | Oxidative Stress > Flashcards

Alcohol Metabolim | Oxidative Stress Flashcards

1
Q

Location of alcohol metabolism

A

Liver 90%
Excited in urine or on breath 10%

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2
Q

Outline alcohol metabolism

A
  • alcohol > acetaldehyde via alcohol dehydrogenase
  • acetaldehyde > acetate via aldehyde dehydrogenase
  • both steps also include NAD+ >NADH
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3
Q

What are the recommend limits for alcohol consumption?

A

14 units/week spread over at least 3 days

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4
Q

What causes a hangover?

A

Accumulation of toxic acetaldehyde

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5
Q

What happens to acetate after alcohol metabolism?

A
  • added to coenzyme A to make acetyl coA
  • metabolised in TCA
  • utiltised for fatty acid synthesis
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6
Q

What are three forms of liver damage due to chronic alcohol consumption?

A

Fatty liver
Alcohol hepatitis
Alcoholic cirrhosis

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7
Q

How can liver damage lead to changes in liver metabolism

A

Excess NADH - decrease in NAD+/NADH ratio
Excess acetyl coA

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8
Q

What are the consequences of liver damage due to chronic alcohol consumption?

A

decrease in NAD+/NADH ratio:
- lactic acidosis
- urate crystals accumulate > gout
- hypoglycaemia

increased acetyl coA
- fatty liver

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9
Q

What is used to treat alcohol dependence?
How does it work?

A

Disulfiram
- Inhibitor of aldehyde dehydrogenase > accumulation of acetaldehyde > toxic > hangover feeling

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10
Q

What conditions can oxidative stress cause?

A

COPD
Crohn’s disease
RA
Alzheimer’s
Ischaemic injury
Cancer
Pancreatitis
Parkinson’s disease
MS
Cardiovascular disease

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11
Q

What is a free radical?

A

An atom that has 1 or more unpaired electrons + is capable of independent existence

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12
Q

What is used to denote a free radical?

A

Superscript dot

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13
Q

Examples of free radicals

A

Hydroxyl radical OH°
Superoxide O2°-
Nitric oxide NO°

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14
Q

Why are free radicals so damaging

A

Very reactive
Reactions generate a second radical > propagating damage

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15
Q

What are the two types of free radicals?

A

Reactive oxygen species
Reactive nitrogen species

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16
Q

How are reactive oxygen species formed

A

O2 + e- > superoxide O2°- > hydrogen peroxide H2O2 > hydroxyl radical OH°

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17
Q

How are reactive nitrogen species formed?

A

Superoxide O2°- + nitric oxide NO° > peroxynitate ONOO-

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18
Q

What are the two main types of damage to DNA of ROS

A

Reacts with base > modifies base causing mispairing + mutation
Reacts with sugar > strand break > possible mutation on repair

19
Q

Outline the damage of ROS to proteins

A
  • backbone > fragmentation > protein degradation
  • sidechain > chains in protein structure > loss or gain of function / protein degradation
20
Q

What are disulphide bonds formed between?

A

Thoil groups on cysteines

21
Q

Outline ROS damage to lipids

A

Lipid peroxidation

Unsaturated lipid + FR > lipid radical
Lipid radical reacts with O2 > lipid peroxyl radical
Process repeats + chain reaction formed

22
Q

3 endogenous sources of biological oxidants

A

Electron transport chain
Nitric oxide synthases
NADPH oxidases

23
Q

Exogenous sources of biological oxidants

A

Radiation - UV, X ray
Pollutants
Drugs - primaquine
Toxins

24
Q

How is the electron transport chain a source of ROS?

A

NADH and FADH2 supply e-
Sometimes e- may escape ETC and react with O2 to form superoxide

25
Q

Explain how nitric oxide synthase acts as an endogenous source of ROS

A

Arginine > citrulline + NO°
nitric oxide synthase

Nitric oxide is toxic in high levels

26
Q

What are the 3 types of nitric oxide synthase?

A

iNOS - inductive nitric oxide synthase
- direct toxic effect in phagocytes
eNOS - endothelial nitric oxide synthase
- produce signalling molecules
nNOS - neuronal nitric oxide synthase
- produce signalling molecules

27
Q

What is respiratory burst?

A
  • Rapid production of superoxide + H2O2 from phagocytic cells
  • ROS and peroxynitrite destroy invading bacteria
  • antimicrobial defence system
28
Q

What does a defect in respiratory burst cause?

A

Chronic granulomatous disease

29
Q

Cellular defences against ROS

A
  • superoxide dismutase - converts superoxide to H2O2 and O2
  • catalse - converts H2O2 into H2O and O2
  • glutathoine GSH - explained on another slide
  • free radical scavengers - vitamin E + C
30
Q

Outline how glutathione (GSH) protects actions ROS

A
  • GSH is oxidised by glutathione peroxidase using selenium cofactor to GSSG
  • this converts H2O2 (from ROS) to H2O
  • GSSG reduced back to GSH by glutathione reductase which uses e- from NADPH from PPP
31
Q

Outline how free radical scavengers defend against ROS

A

Vitamin E - protection against lipid peroxidation
Vitamin C - role in regenerating reduced from of vitamin E

32
Q

What is the rate limiting enzyme in the pentose phosphate pathway?

A

Glucose 6 phosphate dehydrogenase

33
Q

What is a clinical sign of G6PDH deficiency?

A

Heinz bodies

34
Q

What are Heinz bodies?

A

Dark staining within RBCs from precipitated haemoglobin > bind to cell membrane + alters rigidity

35
Q

What does G6PDH deficiency cause?

A

Less NADPH
NAPDH is required to reduce GSSG to GSH
Less protection from oxidative stress
Lipid peroxidation + protein damage
Haemolysis

36
Q

Outline paracetamol metabolism

A
  • at a safe level it is broken down into glucuronide + sulphate
  • at high levels it is broken down into NAPQI > direct toxic effects on protein, DNA and damage
  • glutathione protects against NAPQI
37
Q

What drug is used to treat paracetamol overdose?
How does it work?

A

Acetycystine
Replenishes glutathione levels which protects against NAPQI

38
Q

How can chronic alcohol consumption cause gout?

A
  • decreased NAD+
  • inadequate NAD+ for lactate > pyruvate
  • ^ lactate
  • lactate competes with uric acid for excretion
  • ^ uric acid levels > urate crystals accumulate
  • gout
39
Q

How can chronic alcohol consumption cause fatty liver?

A
  • increased acteyl-CoA > increased synthesis of fatty acids
  • decreased NAD+ > reduced fatty acid oxidation
  • both cause increased synthesis of triacylglycerol
  • fatty liver
40
Q

How is a superoxide formed?

A

O2 reacts with e-

41
Q

What is chronic granulomatous disease?

A
  • Genetic defect in NADPH oxidase complex
  • Respiratory burst compromised
  • Causes enhanced susceptibility to bacterial infections
42
Q

How does superoxide dismutase and catalase defend against free radicals?

A
  • SOD converted superoxide to H2O2 + O2
  • catalase converts H2O2 to H2O and O2
43
Q

What property of aldehyde dehydrogenase limits the toxic effects of acetaldehyde?

A

Has a low Km of acetaldehyde

44
Q

How do free radical scavengers help prevent oxidative stress?

A

Donate hydrogen atom + electron in ROS/RNS in non enzymatic reaction

MEH (23 decks)

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