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Life protection > Cell death and cell damage > Flashcards

Cell death and cell damage Flashcards

1
Q

What are the 3 basic mechanisms which cause cell death?

A
  1. Necrosis
  2. Apoptosis
  3. Autophagic cell death
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2
Q

What are the causes of necrosis?

A
  • Usually caused by lack of blood supply to cells or tissues, e.g.
  • injury,
  • infection,
  • cancer,
  • infarction,
  • inflammation
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3
Q

What are the steps involved in necrosis?

A
  1. Whole groups of cells are affected.
  2. Result of an injurious agent or event.
  3. Reversible events proceed irreversible
  4. Energy deprivation causes changes. (e.g. cells unable
    to produce ATP because of oxygen deprivation)
  5. Cells swell due to influx of water (ATP is required for ion
    pumps to work).
  6. Haphazard destruction of organelles and nuclear
    material by enzymes from ruptured lysosomes.
  7. Cellular debris stimulates an inflammatory cell response
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4
Q

What are the nuclear changes of a cell in necrosis?

A
  1. Chromatin condensation/shrinkage.
  2. Fragmentation of nucleus.
  3. Dissolution of the chromatin by DNase causing a fading in
    the basophillia of the chromatin.
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5
Q

What are the cytoplasmic changes of cells in necrosis?

A
  1. Opacification: denaturation of proteins with aggregation.
  2. Complete digestion of cells by enzymes causing cell to liquify
    (liquefactive necrosis).
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6
Q

What are the biochemical changes of a cell in necrosis?

A
  1. Release of enzymes such as creatine kinase or lactate dehydrogenase
  2. Release of proteins such as myoglobin
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7
Q

What are examples of clinical investigations associated with cell death?

A
  1. Muscular dystrophy
  2. Heart attack
  3. Bone and liver disease
  4. Haemolytic anaemias
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8
Q

What do damaged muscles release in muscular dystrophy?

A

Damaged muscles release creatine
kinase and lactate dehydrogenase (M3 and M3H isoforms)

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9
Q

What do damaged muscle cells release in heart attacks?

A

Damaged muscle cells release lactate
dehydrogenase (H3 and H3M isoforms).

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10
Q

What do damaged tissues release in bone and liver diseases?

A

Damaged tissues release alkaline
phosphatase and lactate dehydrogenase isoforms (different
isoforms specific to various tissues)

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11
Q

What do damaged red cells release in haemolytic anaemia?

A

Damaged red cells release LDH1/2

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12
Q

What are the different types of necrosis?

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Fatty necrosis
  5. Fibrinoid necrosis
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13
Q

Where is coagulative necrosis typically seen>

A

typically seen in hypoxic environments

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14
Q

What does coagulative necrosis look like under a light microscope?

A

Cell outlines remain after cell death and can be observed by light
microscopy

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15
Q

What is liquefactive necrosis associated with?

A

Is associated with cellular destruction and pus
formation (e.g. pneumonia)

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16
Q

What is caseous necrosis a mix of?

A

Is a mix of coagulative necrosis and liquefactive necrosis like TB

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17
Q

What is fatty necrosis the result from?

A

Results from the action of lipases on fatty tissues (e.g. acute
pancreatitis)

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18
Q

What is fibrinoid necrosis caused by?

A

Caused by immune-mediated vascular damag

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19
Q

What is fibrinoid necrosis marked by and what does it appear as?

A

It is marked by deposition of fibrin-like proteinaceous material in arterial
walls, which appears smudgy and acidophilic on light microscopy.

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20
Q

What is the overall function of necrosis?

A

Removes damaged cells from an organism

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21
Q

What can failure of necrosis lead to?

A

Lead to chronic inflammation

22
Q

What is the function of apoptosis?

A

Selective process for the deletion of superfluous,
infected or transformed cells

23
Q

What are factors influencing the balance of life and death at the cellular level?

A
  1. Cell-cell and/or cell-matrix contacts
  2. Growth factors
  3. Cytokines
  4. Disruption of cell-cell and/or cell-matrix contacts
  5. Lack of growth factors
  6. DNA damaging events
  7. Death domain ligands
24
Q

What are the 2 types of pathway and what triggers each one?

A

Intrinsic
-DNA damage-p53 dependent pathway
Extrinsic
-Extracellular signals like TNF

25
Q

What happens in intrinsic apoptosis?

A
  1. Interruption of the cell cycle
  2. Inhibition of protein synthesis
  3. Change in redox state
  4. Withdrawal of growth factors like IL-3
26
Q

What happens in extrinsic apoptosis?

A

T cell or NK (Natural Killer) (e.g. Granzyme).

27
Q

What are caspases?

A

Caspases are Cysteine Proteases that play a central
role in the initiation of apoptosis

28
Q

How are most proteases synthesised and how are they usually activated?

A

Most proteases are synthesised as inactive
precursors requiring activation (usually partial
digestion by another protease).
(Cysteine Aspartate-specific Proteases)

29
Q

What are the steps involved in the intracellular proteolytic cascade in procaspase activation?

A
  1. Inactive procaspase Y has cleavage sites
  2. Activation occurs by cleavage leading to the formation of active caspase X and a prodomain
  3. Leads to activate caspase Y with large subunit and small subunit
30
Q

What are the steps involved in the caspase cascade?

A
  1. There’s an active initiator caspase
  2. Cleavage of cytosolic protein which leads to the formation of many molecules of active caspase Y
  3. Cleavage of nuclear lamina from the many molecules of active caspase-Y leads to even more molecules of active caspase-Z
31
Q

What does caspase activation lead to?

A

Caspase activation leads to characteristic morphological
changes of the cell such as shrinkage, chromatin
condensation, DNA fragmentation and plasma membrane
blebbing.

32
Q

What are the steps involved in apoptosis?

A
  1. Single or few cells selected
  2. Programmed cell death
  3. Irreversible once initiated
  4. Events are energy driven
  5. Cells shrink as the cytoskeleton is disassembled
  6. Orderly packaging of organelles and nuclear fragments in membrane bound vesicle
  7. New molecules expressed on vesicle membranes stimulate phagocytosis, no inflammatory response
33
Q

How do the nuclear changes of apoptosis appear under a microscope?

A
  1. Nuclear chromatin condenses on nuclear membrane.
  2. DNA cleavage.
34
Q

How do cytoplasmic changes of apoptosis appear under a microscope?

A
  1. Shrinkage of cell. Organelles packaged into membrane vesicles.
  2. Cell fragmentation. Membrane bound vesicles bud off.
  3. Phagocytosis of cell fragments by macrophage and adjacent cell.
  4. No leakage of cytosolic components.
35
Q

How do we activate the initiator caspases?

A

By induced proximity.

35
Q

What does TNF induce the formation of?

A

TNF induces the formation of a
death-inducing signalling complex
= DISC

35
Q

How do biochemical changes of apoptosis appear under a microscope?

A
  1. Expression of charged sugar molecules on outer and inner surface of membranes (recognised by macrophage and enhances phagocytosis
  2. Protein cleavage by proteases, caspases
36
Q

What are the steps involved in the extrinsic pathway of ligand induced dimerisation in apoptosis?

A
  1. TNF binds to TNFR which has a death domain
  2. Triggers death domain on FAAD, which has a death effector domain
  3. This triggers the death effector domain on the procaspase-8 which has a protease domain
  4. This results in autoproteolysis
37
Q

What is cytochrome C?

A

Mitochondrial matrix protein

38
Q

What is cytochrome C released in response to?

A

To be released in response
to oxidative stress by a “permeability transition”

39
Q

What do any inducers of permeability transition also eventually induce?

A

Any inducers of the permeability transition also
eventually induce apoptosis.

40
Q

What is the intrinsic pathway of cytochrome C-induced apoptosis?

A
  1. Cytochrome-C binds to cytochrome C binding site on APAF-1 which has a APAF domain and a caspase recruitment domain(CARD)
  2. The CARD domian on procaspase-9 is triggered which also has a protease domain which results in autoproteolysis
41
Q

What does cytochrome C induce?

A

Cytochrome c induces the formation of a
death-inducing complex

42
Q

What is bcl-2 a member of?

A

bcl-2 is a member of a multi-gene
family in mammals

43
Q

What are examples of anti-apoptotic genes?

A

Bcl-2, Bcl-XL

44
Q

What are examples of pro-apoptotic genes?

A

Bax, Bad and Bid

45
Q

How is the release of cytochrome C regulated?

A

Bax directly induces release of cytochrome c from isolated mitochondria

46
Q

What does Bcl2 do to regulate release of cytochrome C?

A

Bcl-2 blocks Bax, preventing cytochrome C from leaving mitochondria

47
Q

How is Bad activated and how does it regulate the release of cytochrome C?

A
  1. Survival signals like AKT/PKB cause Bad to be dephosphorylated, hence in its activated form
  2. Bad binds to Bcl-2 which allows Bax to release cytochrome C
  3. Cytochrome C activates APAF/Caspase-9 leading to cell death
48
Q

How does intracellular stress lead to cell death?

A
  1. Intracellular stress leads to transcription by p53
  2. This activates Bax which is inserted into the mitochondrial membrane
  3. This causes cytochrome-C release which activates APAF/caspase-9
  4. Leads to cell death
49
Q

What do some mutations in p53 destroy the ability of?

A

Some mutations destroy the ability of p53 to induce
Apoptosis.

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