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CVDM > Reactive Oxygen Species > Flashcards

Reactive Oxygen Species Flashcards

1
Q

What are reactive oxygen species?

A

Highly reactive metabolites of molecular oxygen

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2
Q

How are reactive oxygen species produced?

A

Primarily a by-product of the incomplete reduction of oxygen in the respiratory chain

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3
Q

How are reactive oxygen species produced?

A

They are a by-product of the incomplete reduction of oxygen in the respiratory chain

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4
Q

Examples of reactive oxygen species

A

Superoxide anion
Hydrogen peroxide
Hydroxyl radical
Peroxinitrite

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5
Q

What are NADPH oxidases?

A

Major source of ROS in the cell

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6
Q

NADPH oxidases contain how many enzymes?

A

They are multimeric enzymes

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7
Q

True or false:
There is only one isoform of the NOX catalytic subunit

A

False - there are many (Nox1-5, Duox1/2)

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8
Q

Is NOX2 active or inactive?

A

It exists in both active and inactive states

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9
Q

What ROS does NOX2 produce?

A

Superoxide

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10
Q

Is NOX4 active or inactive?

A

Constituently active

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11
Q

What ROS does NOX4 produce?

A

Hydrogen peroxide

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12
Q

NOX2 and NOX4 produce high/low levels of ROS

A

Low

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13
Q

What roles does NOX2 play in CVD?

A

Atherosclerotic lesion formation
Determining size of infarct after ischaemic reperfusion injury
Calcium release from SR

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14
Q

What does NOX4 protect the vasculature against?

A

Inflammatory stress

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15
Q

How are ROS generated from NOX2?

A

Physiological stretch activates activates NOX2 generating ROS

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16
Q

Where does ROS production take place?

A

Sarcolemmal and T-tubule membranes

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17
Q

True or false:
ROS production triggers the release of calcium sparks?

A

True, they are mediated via RyR in the SR

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18
Q

Stretch increases/decreases the frequency of sparks?

A

Increases

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19
Q

Is the activity of the RyR redox sensitive?

A

Yes

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20
Q

How is the LTCC inhibited?

A

By oxidation as it is redox sensitive

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21
Q

Free radicals inhibit/potentiate LTCC?

A

Inhibit

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22
Q

What is the effect of chemical oxidation of sodium channels?

A

It impairs their rapid inactivation, meaning there is a longer depolarising current, a longer action potential and this can lead to arrhythmogenesis and sodium overload

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23
Q

Effect of oxidants such as H2O2 on SERCA and the NCX

A

Inhibit SERCA
Activate NCX

24
Q

How does H2O2 reduce the size of the calcium transient?

A

H2O2 enhances removal of calcium from cells and reduces calcium re-uptake into SR
Calcium content of SR becomes more and more empty, leading to the reduction in size of the calcium transient

25
Q

What is glutathionylation?

A

Post-translational modification in which glutathione reversibly binds to thiol groups on proteins via disulphide bonds

26
Q

What is glutathione?

A

A cellular reducing agent

27
Q

Which subunit of the Na pump undergoes glutathionylation under oxidative stress to reduce its activity

A

The beta subunit

28
Q

ROS are positively/negatively inotropic?

A

Negatively inotropic, depress cardiac contractility

29
Q

How does ROS reduce the size of the calcium current?

A

By activating the RyR, depleting the SR of Ca
Inhibits the LTCC

30
Q

How does ROS prolong the AP?

A

Slows the inactivation of LTCC

31
Q

Which type of PKA is redox active?

A

Type I PKA

32
Q

How is PKA I activated?

A

Activated by hydrogen peroxide which promotes the formation of disulphide bond between 2 regulatory subunits

33
Q

Voltage gated calcium channels:
What are they phosphorylated by?
What is the effect of the phosphorylation?

A

Phosphorylated of Rad by PKA
Increases trigger calcium and increases CACR

34
Q

RyR:
What are they phosphorylated by?
What is the effect of the phosphorylation?

A

Phosphorylated by PKA
Increases calcium release from SR

35
Q

SERCA2a/PLB:
What is it phosphorylated by?
What is the effect of the phosphorylation?

A

PLB phosphorylated by PKA
Increases SERCA activity, increasing Ca reuptake into SR, increasing Ca store and gives rise to bigger calcium transients

36
Q

Sodium pump:
What is it phosphorylated by?
What is the effect of the phosphorylation?

A

PLM phosphorylated by PKA
Increases Na efflux, preventing Na overload

37
Q

Troponin I:
What is it phosphorylated by?
What is the effect of the phosphorylation?

A

TnI phosphorylated by PKA
Reduced affinity of TnC for Ca, reduction in contraction of cardiac muscle and accelerates relaxation

38
Q

Biochemical changes ischaemia

A

Switch to anaerobic ATP production
Metabolite accumulation

39
Q

Which metabolites accumulate in ischaemia?

A

Protons (cause acidosis)
Phosphate
Free radicals
Potassium
Oxidised lipids

40
Q

What happens in the baroreceptor reflex?

A

Increased sympathetic stimulation
Increased contractility
Increased oxygen demand

41
Q

How does impaired pumping accelerate glycolysis?

A

Briefly increases glucose uptake into myocyte
Inhibits glycogen synthetase
Activates phosphofructokinase reaction

42
Q

Why does glycolysis fail under ischaemic conditions?

A

Lack of substrate to metabolise
Lack of oxidised NAD
Metabolic acidosis

43
Q

Consequences of metabolic acidosis in ischaemica

A

Inhibition of NCX and RyR (this is protective)
Reduces action potential velocity
Protons compete with Ca for binding to specific sites on proteins

44
Q

Acidosis occurs quickly/slowly after the onset of ischaemia

A

Very quickly

45
Q

Acidosis occurs quickly/slowly after the onset of ischaemia

A

It occurs extremely rapidly

46
Q

What is the primary explanation for impaired heart contractility in ischaemia?

A

Acidosis reduces calcium affinity, maximum tension and contractility of myofilaments

47
Q

Function of NCX

A

Regulates intracellular pH through exchange of intracellular H+ for extracellular Na

48
Q

What is HNE?

A

A major lipid peroxidation product formed during oxidative stress

49
Q

What does HNE do?

A

Reacts with thiol groups on proteins altering their activities

50
Q

What is the garden hose effect?

A

Perfusion of the intracoronary vessels has a distending effect on the cardiac muscle, distension of the cardiac muscle is positively inotropic

51
Q

How does impaired relaxation arise in early and late ischaemia?

A

Early - inhibition of Ca efflux
Late - formation of rigor bonds

52
Q

Changes to the cardiac action potential in ischaemia

A

Delayed activation
Slower to rise (due to less Na channels in resting state)
Slower to trigger Ca channels
Reaches threshold more slowly
AP propagates more slowly

53
Q

What causes cells to die in ischaemia?

A

Calcium activated proteases degrade proteins and long chain AcylCoA disrupts sarcolemma

54
Q

What is reperfusion injury?

A

Restoration of blood flow following ischaemia results in a substantial increase in number of cardiomocytes that die

55
Q

What causes reperfusion injury?

A

Abnormal calcium handling
Oxidative stress
Mitochondrial dysfunction

56
Q

Mitochondrial Permeability Transition Pore (mPTP) opening is acclelerated/decelerated by Ca and Ros

A

Accelerated

57
Q

Myocytes appear to be ___ years younger than the person they’re from?

A

10 years younger

CVDM (16 decks)

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