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MEH > Alcohol metabolism and ox stress > Flashcards

Alcohol metabolism and ox stress Flashcards

1
Q

Where is alcohol metabolised

A

90% metabolised in liver
remainder excreted passively by urine or breath

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2
Q

what is the recommended unit limit of alcohol a week

A

14 units for both men and women spread over at least three days

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3
Q

what is the rate of alcohol metabolism

A

7g per hour

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4
Q

how many grams is one unit of alcohol

A

8g

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5
Q

what does is mean that rate of alcohol metabolism is zero order

A

means that a change of conc does not change rate

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6
Q

what is the first step and enzyme in alcohol metabolism

A

Enzyme: alcohol dehydrogenase
alcohol converted to acetaldehyde using NAD to produce NADH

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7
Q

why is a build up of acetaldehyde a problem

A

it is toxic so causes hangover like symptoms

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8
Q

what does it mean that alcohol dehydrogenase is low specificity

A

low Km so high affinity even at low concs

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9
Q

what is the second enzyme and step in alcohol metabolism

A

enzyme: aldehyde dehydogenase
converts acetaldehyde to acetate using NAD to NADH which is then conjugated to CoA

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10
Q

what can a small amount of alcohol by metabolised by

A

cytochrome P450ZE1 or catalase in the brain

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11
Q

how can excessive alcohol consumption damage the liver membranes and what enzymes appear in blood to show this

A
  • pathways saturated so acetaldehyde accumulates which is toxic
  • this causes liver cells to have more leaky membranes which causes a loss of enzymes (enzymes like transaminases and gamma glutamyl transpeptidase appear in blood )
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12
Q

how is the damaged liver from alcohol consumption not able to function

A
  • reduced ability to take up billirubin leading to hyperbillirubinaemia leading to jaundice
  • high ammonia and glutamate
  • low albumin levels, lotting factors and lipoproteins so lipids synthesised in liver cannot be transported out –> fatty liver
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13
Q

how does alcohol oxidation affect liver metabolism by having increased acetyl CoA

A

increased synthesis of fatty acids and ketone bodies so more triacylglycerols more fatty liver

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14
Q

how does alcohol oxidation affect liver metabolism by having decreased NAD

A
  • not enough NAD for conversion of lactate to pyruvate so lactate accum in blood –> lactic acidosis and kidney has same transporters for lactate and urea so saturated with lactate so urea builds up –> gout
  • inadequate NAD for glycerol metabolism so deficit in gluconeogenesis leading to hypoglycaemia
  • not enough NAD for fatty acid ox so more triacylglyerols
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15
Q

how does excess alcohol affect GI tract

A
  • damage to cells lining GI
  • low appetite, diarrhoea, impaired absorption (vit K, folic acid, pyridoxine, thiamine –> Korsakoff’s)
  • chronic pancreatitis
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16
Q

what is disulfiram

A

a drug that is used as a adjunct to treat chronic alcohol dependence

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17
Q

describe the mechanism of disulfiram

A
  • inhibits the enzyme aldehyde dehydrogenase
  • accumulation of acetaldehyde
  • symptoms of hangover –> classical conditioning
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18
Q

what is a free radical

A

any atom or molecule or ion that has one or more unpaired electrons and capable of independent existence

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19
Q

what are properties of free radicals

A
  • very reactive
  • tend to acquire electrons from other molecules causing damage and generating new radicals = chain reaction
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20
Q

how is the ROS superoxide formed

A

oxygen + e –> superoxide

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21
Q

why is oxygen considered a biradical

A

has two unpaired electrons

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22
Q
A
23
Q

how do ROS damage DNA when reacting with a sugar

A

cause strand breaking or mutation leading to cancer

23
Q

how do ROS damage DNA when reacting with a base

A

cause mispairing and mutation leading to cancer

24
Q

how do ROS damage proteins when reacting with the sidechain

A

modified AA gives rise to diff structure which leads to loss of function degradation, gain of new function

24
Q

how do ROS damage proteins when reacting with the backbone

A

fragmentation of backbone leads to protein degredation

25
Q

how do ROS cause damage by forming disulphide bonds

A
  • ROS can cause extra disulphide bonds
  • form between thiol groups of cysteine residues
  • ROS takes electrons from cysteines causing misfolding and cross linking
26
Q

how do ROS damage lipids

A
  • free radical extract H+ from polyunsaturated FA in mem which forms a radical which can react with oxygen to lipid peroxyl radical = chain reaction of lipid peroxidation
  • causes damage to hydrophobic bilayer of mem so integrity of mem fails
27
Q

what are the endogenous sources of ROS

A
  • ETC electron escapes and reacts with oxygen
  • peroxidases
  • nitric oxide synthases
  • lipooxygenases
  • NADPH oxidases
  • xanthine oxidase
  • monoamine oxidase
28
Q

what are some exogenous source of ROS

A
  • Radiation (UV, cosmic, X- rays)
  • pollutants
  • drugs (primaquine)
  • toxins (paraquat)
29
Q

lists the ROS

A
  • superoxide
  • hydrogen peroxide
  • hydroxyl radical
30
Q

list the RNS

A
  • peroxynitrite
  • nitric oxide
31
Q

how is hydrogen peroxide formed

A

superoxide + 2H+ + e –> H2O2

32
Q

how is the hydroxyl radical formed

A

H2O2 + e + H+ –> H2O + OH

33
Q

how is nitric oxide formed

A
  • from arginine and NADPH and O2 using nitric oxide synthase
34
Q

what are the three isoforms of nitric oxide synthase

A
  • iNOS ( inducible) : produced high NO in phagocytes for resp burst
  • eNOS ( endothelial): signalling
  • nNOS (neuronal) : signalling
35
Q

how is peroxynirite formed

A

nitric oxide reacts with superoxide to produce peroxynitrite

36
Q

what is the respiratory burst

A

rapid production of superoxide and H2O2 from phagocytic cells so ROS and peroxynitrite can destroy bacteria invading cells

37
Q

describe the process of respiratory burst

A
  • phagolysosome engulfs invading bacteria
  • NADPH oxidase converts NADPH + O2 –> NADP and forms superoxide which converts to H2O2
  • superoxide reacts with nitric oxide made by iNOS to form peroxynitrite
  • H2O2 reacts with Cl- catalysed myleoperoxidase to make hypochlorite
  • hypochlorite and peroxynitrite destroy invading bacteria
38
Q

how does the enzyme superoxidase dismutase protect against ROS

A

converts superoxide to H2O2 and O2

  • primary defence (especially in ETC) as superoxidase is strong inhibitor
  • 3 isoforms
39
Q

how does catalase protect against ROS

A

converts H2O2 to water and oxygen
- important in immune cells to protect against widespread burst

40
Q

what is glutahtione

A

a tripeptide synthesised by body to protect against ox damage

41
Q

what three AA make up glutathione

A

gly- cys- glu

42
Q

how does glutathione protect against ox damage using what enzyme

A

thiol group on cys donates electron to ROS then reacts with another GSH forming disulphide bonds (GSSG) catalysed by enzyme glutathione peroxidase which requires selenium

43
Q

how is GSSG reduced back to GSH

A

GSH is reduced active form so converted using enzyme glutathione reductase which transfers electrons from NADPH ( from PPP) to disulphide bond

44
Q

what are free radical scavengers

A

reduce free radicals damage by donating hydrogen atoms and an electron to free radicals in nonenzymatic reaction

45
Q

name the free radical scavengers

A
  • vitamin E
  • vitamin C
  • carotenoids
  • flavonoids
  • uric acid
  • melatonin
46
Q

how is ox stress caused in galacosemia

A
  • deficiency in an enzyme in galactose pathway
  • build up of galactose converted to galacticol by aldose reductase consuming excess NADPH
  • lower NADPH means less defence from ROS and cannot convert GSSG back to GSH
  • disulfide bonds form in lens
47
Q

how does a deficiency in G6PD enzyme relate to ox stress

A

G6PD enzyme in PPP so no NADPH formed so GSSG cannot be converted to GSH so less protection

48
Q

how are heinz bodies formed

A
  • ROS cross links Hb forming aggregates
49
Q

how is paracetamol normally metabolised

A

broken down in liver to glucuronide and sulphate

50
Q

what happens to paracetamol metabolism when overdosing

A

normal pathway saturated so go down NAPQI pathway which is directly toxic (ROS) to cells and depletes cells of glutathione causing more ox damage

51
Q

what is the antidote for paracetamol overdose and how does it work

A
  • acetylcysteine
    replenishes glutathione levels to protect against ox stress

MEH (12 decks)

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