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Biology Of Ageing Year2 > Oxidative Stress > Flashcards

Oxidative Stress Flashcards

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1
Q

What is the major driver of ageing?

A

Oxidative stress causes the most damage/stress in relationship to ageing.

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2
Q

What is the free radical theory?

A

Oxygen is toxic chemically because it can form free radicals. This is occurs due to respiration.

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3
Q

What is a free radical?

A

An uncharged molecule (typically highly reactive and short-lived) having an unpaired valency electron.

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4
Q

Where are most free radical produced?

A

Mitochondria

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5
Q

What is Reactive Oxygen Species (ROS)?

A

Oxygen-centred free radicals plus molecules that contribute to their formation.

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6
Q

What is oxidative stress?

A

Oxidative stress is the imbalance between pro-and antioxidants in the cell, leading to accumulation of oxidative damage.

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7
Q

What is the reactivity of superoxides?

A

High

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8
Q

What is the reactivity of hydrogen peroxide?

A

Low

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9
Q

What is the reactivity of the hydroxyl radical?

A

Very high

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10
Q

What is the half-life of superoxides?

A

That is concentration dependent.

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11
Q

What is the half-life of hydrogen peroxide?

A

Seconds to minutes

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12
Q

What is the half life of hydroxyl radical?

A

Milliseconds

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13
Q

What is superoxide soluble in?

A

Water

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14
Q

What is hydrogen peroxide soluble in?

A

Water and lipids

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15
Q

What are hydroxyl radicals soluble in?

A

Water

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16
Q

What does a high reactivity mean for a free radical?

A

Shorter half life.

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17
Q

Why is it important that superoxides are soluble in water?

A

They cannot cross membranes.

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18
Q

What is important about hydrogen peroxide (H2O2)?

A

Although it has low reactivity however can travel around as it is soluble in water and lipids which means it can act as a messenger for reactive species.

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19
Q

Why are hydroxyl radicals not a huge risk inside the body?

A

Such a small half life it wouldn’t have time to cause damage.

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20
Q

Where is nitric oxide synthase?

A

Cytoplasm.

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21
Q

Where are superoxides formed?

A

Inner matrix of the inner mitochondria.

Can also be other membrane bound organelle like exosomes.

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22
Q

Why do superoxides accumulate?

A

Cannot cross membranes, so stays within the particle matrix.

23
Q

How is superoxide accumulation solved?

A

Superoxide dismutase (manganese centred) can convert them to hydrogen peroxide which can move through membranes.

24
Q

How is a hydrogen peroxide accumulation prevented?

A

A fentol reaction leads to a hydroxyl radical which then has a short half life and is broken down.

25
Q

What are antioxidants?

A

Cells primary defence against ROS.

26
Q

What kinds of antioxidants are there?

A

Enzymatic

Non-enzymatic “scavengers”

Metal chelators

27
Q

Examples of enzymatic antioxidants?

A

– Superoxide dismutases
– Catalase
– Glutathion peroxidases
– Thioredoxins

28
Q

What kinds of non-enzymatic, “scavengers”, antioxidants are there?

A

Lipid soluble

Water soluble

29
Q

What kinds of lipid soluble, non-enzymatic “scavengers”, antioxidants are there?

A

VitE
Carotenoids
Q10

30
Q

What kinds of water soluble, non-enzymatic “scavengers”, antioxidants are there?

A

VitC
GSH
uric acid

31
Q

What is GSSG replenished by?

A

NADPH.

32
Q

What is GPI?

A

Detoxifying pathway.

33
Q

What are the cellular secondary defences of DNA repair?

A

Base excision repair (BER)

Nucleotide excision repair (NER)

Mismatch repair

Double stranded break repair

34
Q

What kind of base excision repair (BER) are there?

A

Nuclear

Mitochondrial

Single strand break

35
Q

What kind of nucleotide excision repair (NER) are there?

A

Transcription- coupled

Genome wide

36
Q

What kind of double strand break repair is there?

A

Non-homologous end joining

Homologous recomination.

37
Q

What is XPD?

A

Helicase subunit of TF2H

38
Q

What is the function of XPD?

A

NER and transcription, mutated in trichodiodystrophy.

39
Q

What is XPA?

A

Necessary for NER but not for transcription

40
Q

What is protein turnover by chaperone-ubiquitin-proteasome system?

A

Damage proteins recognised by ligase ubiquitin activated, rest of protein moves onto the proteosome.

41
Q

What happens to protein turnover by chaperone-ubiquitin-proteasome system with age?

A

Can lose efficiency with age.

42
Q

What is the process of protein turnover by lysosomal system?

A

Recognises damaged organelle, encapsulates them in an autophagosome, organelle is degraded and its components are reused.

43
Q

What is the autophagosome?

A

Single membrane vesicle which fuses with the lysosome.

44
Q

What changes in protein turnover by lysosome?

A

Lysosomes get fuller until they become damaged and release lysosomal contents.

45
Q

What is the issue with old age lysosomes?

A

Contribute to cellular dysfunction.

46
Q

What is a telomere?

A

Define and protect the ends of all linear chromosomes, all animals have them.

47
Q

What happens to telomeres with age?

A

Shorten.

48
Q

Why do telomeres shorten with age?

A

Due to huge amounts of replication, oxidative stress induces this.

49
Q

What is important about telomeres?

A

Could be how we quantify ageing.

Association with stress depending disaeses.

50
Q

What happens when you genetically modify polymerase gamma (polyG)?

A

Proofreading in ribosome is now not functioning.
The information transcribed but it carries mistakes.
Lowered the effect of ageing but more oxidative stress.

51
Q

Do antioxidants extend life?

A

No. They are good for you though.

52
Q

What is PRX?

A

peroxiredoxin

53
Q

What is SRX?

A

Sulfiredoxin

54
Q

What is SO2H

A

Sulfinic acid.

Biology Of Ageing Year2 (23 decks)

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