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MEH > Alcohol Metabolim | Oxidative Stress > Flashcards

Alcohol Metabolim | Oxidative Stress Flashcards

(44 cards)

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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

Study These Flashcards
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

Study These Flashcards
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?

Study These Flashcards
A

Thoil groups on cysteines

21
Q

Outline ROS damage to lipids

Study These Flashcards
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

Study These Flashcards
A

Electron transport chain
Nitric oxide synthases
NADPH oxidases

23
Q

Exogenous sources of biological oxidants

Study These Flashcards
A

Radiation - UV, X ray
Pollutants
Drugs - primaquine
Toxins

24
Q

How is the electron transport chain a source of ROS?

Study These Flashcards
A

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

25
Explain how nitric oxide synthase acts as an endogenous source of ROS
Arginine > citrulline + NO° *nitric oxide synthase* Nitric oxide is toxic in high levels
26
What are the 3 types of nitric oxide synthase?
**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
What is respiratory burst?
- Rapid production of superoxide + H2O2 from phagocytic cells - ROS and peroxynitrite destroy invading bacteria - antimicrobial defence system
28
What does a defect in respiratory burst cause?
Chronic granulomatous disease
29
Cellular defences against ROS
- **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
Outline how glutathione (GSH) protects actions ROS
- 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
Outline how free radical scavengers defend against ROS
**Vitamin E** - protection against lipid peroxidation **Vitamin C** - role in regenerating reduced from of vitamin E
32
What is the rate limiting enzyme in the pentose phosphate pathway?
Glucose 6 phosphate dehydrogenase
33
What is a clinical sign of G6PDH deficiency?
Heinz bodies
34
What are Heinz bodies?
Dark staining within RBCs from precipitated haemoglobin > bind to cell membrane + alters rigidity
35
What does G6PDH deficiency cause?
Less NADPH NAPDH is required to reduce GSSG to GSH Less protection from oxidative stress Lipid peroxidation + protein damage Haemolysis
36
Outline paracetamol metabolism
- 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
What drug is used to treat paracetamol overdose? How does it work?
*Acetycystine* Replenishes glutathione levels which protects against NAPQI
38
How can chronic alcohol consumption cause gout?
- decreased NAD+ - inadequate NAD+ for lactate > pyruvate - ^ lactate - lactate competes with uric acid for excretion - ^ uric acid levels > urate crystals accumulate - gout
39
How can chronic alcohol consumption cause fatty liver?
- **increased acteyl-CoA** > increased synthesis of fatty acids - **decreased NAD+** > reduced fatty acid oxidation - both cause increased synthesis of triacylglycerol - fatty liver
40
How is a superoxide formed?
O2 reacts with e-
41
What is chronic granulomatous disease?
- Genetic defect in NADPH oxidase complex - Respiratory burst compromised - Causes enhanced susceptibility to bacterial infections
42
How does superoxide dismutase and catalase defend against free radicals?
- SOD converted superoxide to H2O2 + O2 - catalase converts H2O2 to H2O and O2
43
What property of aldehyde dehydrogenase limits the toxic effects of acetaldehyde?
Has a low Km of acetaldehyde
44
How do free radical scavengers help prevent oxidative stress?
Donate hydrogen atom + electron in ROS/RNS in non enzymatic reaction

MEH (23 decks)

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