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Metabolism, Haematology, And Endocrinology > Oxidative stress and alcohol metabolism > Flashcards

Oxidative stress and alcohol metabolism Flashcards

1
Q

Where is the majority of alcohol metabolised? By what and where is a small amount metabolised? Also, what two mechanisms does alcohol pass the metabolism?

A

In the liver

Small amount metabolised by cytochrome p450 and catalase in the brain

some lost in breath and urine

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2
Q

Describe the alcohol metabolism. Products, enzymes and what is produced as well>

A

alcohol–>acetaldehyde–>acetate
Alcohol dehydrogenase
aldehyde dehydrogenase

In the process, NAD+–>NADH

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3
Q

What chemical causes a hangover?

A

acetaaldehyde

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4
Q

What two things does acetate go on to do?

A

TCA cycle or FA synthesis

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5
Q

what metabolite causes liver damage. What three conditions can excessive alcohol consumption lead to?>

A

Acetaldehyde
Fatty liver
alcoholic hepatitis
alcoholic cirrhosis

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6
Q

Describe the metabolic changes that occur due to alcohol consumption (Due to two factors)

A

Decreased NAD+:NADH ratio
Leads to…
-Decreased conversion of Lactate to pyruvate –>increased lactate concentration of the blood–>lactic acidosis
Also increased lactate concentration–>the kidneys ability to remove uric acid to decrease–>urate crystals to build up–>gout

  • Decreased NAD+ for glycerol metabolism–>Less gluconeogenesis–>Hypoglycaemia
  • Less NAD+ for fatty acid oxidation–>increased synthesis of TAGs–>Fatty liver

Also increased Acetyl coA
-Increased FA synthesis–>Increased TAG–>Fatty liver

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7
Q

Describe a treatment for alcohol dependence?

A

Disulfiram

Inhibits aldehyde dehydrogenase, so acetaldehyde build up–>hangover whilst drinking

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8
Q

Name four diseases linked to oxidative stress

A

Cancer
Crohns disease
Cardiovascular disease
Ischaemic/reperfusion injury

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9
Q

Define free radical

A

an atom or molecule that contains one or more unpaired electrons and is capable of free existence

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10
Q

Name 3 ROS and 2 Reactive nitrogen species

A

ROS- Superoxide, Hydrogen peroxide and Hydroxyl radicals

RNS- Nitric oxide and peroxynitrite (ONOO-)

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11
Q

Two main types of damage of ROS to DNA?

A

ROS reacts with base–>mispairing and mutation

ROS reacts with sugar(Ie ribose or deoxyribose)–>strand break and mutation on repair

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12
Q

Explain how ros can damage proteins

A

Can damage backbone or sidechain

to backbone, can cause fragmentation–>protein degradation

to sidechain–>Can modify amino acids by eg. adding disulphide bonds, dimers, carbonyls etc..
leads to change in protein structure–>protein degradation, loss of function or gain of function

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13
Q

What types of groups do disulphide bonds form between?

A

Thiol groups on cysteine residues

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14
Q

What three things can inappropriate disulphide bond formation lead to?

A

Misfolding, cross linking and disruption of function

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15
Q

How can ROS damage lipids?

A

Free radical takes hydrogen atom from a polyunsaturated FA in the membrane lipid

Causes a chain reaction

The hydrophobic enviroment and bilayer gets disrupted and membrane integrity fails

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16
Q

Name three endogenous sources of biological oxidants and three exogenous sources

A

Endogenous: Electron transport chain
Nitric oxide synthases
NADPH oxidases

Exogenous: Radiation (EG. Cosmic rays, X-rays)
drugs
toxins

17
Q

Explain how the electron transport chain can be a source for biological oxidants

A

NADH and FADH2 supply electron
pass through the elctron transport chain
can occasionally escape chain and react with dissolved oxygen–>superoxide

18
Q

What enzyme can make Nitric oxide? What three things is nitric oxide used for? How is nitric oxide made?

A

Nitric oxide synthase
Arginine converted to citrulline and Nitric oxide

Nitric oxide used for: Vasodilation
neurotransmission
S-Nitrosylation

Toxic at high levels

19
Q

What is a respiratory burst?

A

Rapid release of superoxide and Hydrogen peroxide from phagocytic cells
destroy invading bacteria

20
Q

What is the cause of chronic granulomatous disease? What can this lead to?

A

Defect in NADPH oxidase complex
leads to enhanced susceptibility to bacterial infections

eg. Pneumonia, abscesses, impetigo, cellulitis

21
Q

Name three cellular defences against ROS

A

Superoxide dismutase
Catalase
Glutathione

22
Q

Explain how superoxide dismutase acts as a cellular defence

A

Converts superoxide to H2O2 and oxygen

23
Q

Explain how catalase acts as a cellular defence

A

Converts H2O2 to water and oxygen

24
Q

Explain how glutathione acts as a cellular defence

A

The thiol group of glutathione donates an electron to the ROS
reacts with another glutathione in the process
-the enzyme glutathione peroxidase catalyses this reaction. Forms GSSG (GSH–>GSSG)

GSSG–>GSH using glutathione reductase. Requires NADPH–>NADP+

25
Q

Why is the pentose phosphate pathway important in celular defences?

A

Provides NADPH for the reduction of GSSG–>GSH

Enzyme Glutathione reductase catalyses this

26
Q

Whhat two vitamins are important cellular defences?

A

vit C and E

27
Q

Describe how galactosemia causes cataracts

A

Galactose accumulates
requires the alternative pathway to be metabolised
aldose reductase convert galactose to galactitol

uses NADPH–>NADP+
so decreased NADPH levels
so less GSSG converted back to GSH

oxidative damage to cystallin protein in the eye

28
Q

Explain how a G6PDH deficiency can lead to more damage from oxidative stress

A

G6PDH converts 2NADP+–>2NADPH
So deficiency in this enzyme–>decreased NADPH
Decreased NADPH means less GSSG converted to GSH
so less protection to oxidative stress

29
Q

What is the clinical sign of G6PDH deficiency?

A

Heinz bodies

30
Q

What is paracetemol normally broken down to at the prescribed dose?

A

Sulphate and glucuronide

31
Q

What builds up and causes damade in a paracetemol overdose? What type of damage does it cause?

A

NAPQI

Oxidative damage

32
Q

What is the treatment for paracetemol overdose?

A

Acetylcysteine

Replenishes glutathione levels to combat oxidative stress

Metabolism, Haematology, And Endocrinology (24 decks)

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