Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nutrition > Cell Death > Flashcards

Cell Death Flashcards

1
Q

Mechanism of extrinsic pathway of apoptosis

A
  1. trigger by binding of ligand to death-R (TNF-R) with Fas (CTL has FasL = recognize self-AG = eliminate self-reactive apopto) -> Fas + FasL = FADD bind procaspase 8 -> caspase 8 -> caspase 3-6-7-12 (effector) -> apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanism of intrinsic apoptotic pathway (mitochondrial)

A

trigger by DNA damage/damage of cytocavitary network -> MOMP -> cytochrome C in cytosol -> binds APAF-1 -> apoptosome formation and activation -> caspase 9 -> caspase 3-6-7-12 -> apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Consequences of increase cytosolic calcium in cell injury

A
  1. Mitochondrial permeability transition = baisse ATP
  2. Activation enzyme
    a) ATPase = baisse ATP
    b) endonuclease = nuclear damage
    c) protease = disrupt membrane and cytoskeleton protein
    d) phospholipase = baisse phospholipids (membrane)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Autophagy mechanism

A
  1. Isolation membrane encloses cytosolic debris (arise from portions of cell membranes within cell (not plasma membrane))
  2. Autophagosome transport in cytosol vvia microtubules
  3. SNARE-like protein = attachement protein to lysosome
  4. Autophagosolysosome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

By what are pyrine and pyrimidine bound

A

hydrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Repair mechanisms of DNA injury

A
  1. Base excision repair = at any point in cycle
  2. Nucleotide excision repair = mends DNA damaged by chemicals, UV, radiation and other mutagens that causes DNA adducts (DNA covalently bound to chemicals)
  3. DNA miscmatch repair = mends erroneous indels, or mismatch base pair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the features of necrosis?

A

Enlarged cell (swelling)
Pycnosis, karryorhexis, karyolysis
Plasma membrane disrupted
Enzymatic digestion of cell contents (moth eaten apparence)
Cytoplasm red = loss of RNA
Adjacent inflammation
Usually pahologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the features of apoptosis?

A

Reduced cell size
Fragmentation of nucleus
Intact cell membrane
Intact cell content, possible apoptotic bodies
No inflammation
Often physiological (also CTL in viral infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do these leaked IC proteins indicate :
1. troponin
2. alkaline phosphatase
3. transaminase

A
  1. troponin = cardiac muscle cell
  2. alkaline phosphatase = bile duct epithelium
  3. transaminase = hepatocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Anti-apoptotic elements in mitochondrial pathway of apoptosis

A

BCL2, BCLX, MCL1 = resides in mitochondria outer membrane = prevent leakage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pro-apoptotic elements in mitochondrial pathway of apoptosis

A

BAX, BAK (BH1-2) activation = oligomerize with membrane = permeability
Regulated apoptosis initiators : BAD, BID, BIM, Puma, Noxa (BH3 only proteins) = sense stress and damage activates BAX/BAD OR bind anti-apopto to block function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Role of Smac/DIABLO

A

enter cytoplasme and neutrolize anti-apopto (IAP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Inhibition of extrinsic pathway of apoptosis

A

Inhibited by FLIP = binds caspase 8 = blocks FADD
some virus produce FLIP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Morphology and mechanism of necroptosis

A

Morpho = similar to necrosis
Mechanism similar to apoptosis (caspase independant) = ligation of TNF-Fas recruits RIPK1, RIPK3 -> phospho MLKL -> translocate from cytosol to plasma membrane = disrupt = necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is ferroptosis

A

Excessive IC Fe or ROS = overwhelm glutathione antioxydant = membrane lipid peroxidation = permeable = necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Consequences of mitochondrial damage

A
  1. ATP depletion (5-10% = widespread effect)
  2. Na/K ATPase reduced = Na enter, K sort = appel d’eau = swelling
  3. Cellular metabolism hausse glycogenolysis = depletion of glycogen = anaerobic = lactic acid = baisse pH = decrease activity of many enzymes
  4. Incomplete phosphorylation = form ROS
  5. Leakage of mitochondrial prots by BAX/BAK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does damage to DNA trigger?

A

trigger p53 = cell arrest in G1 + active DNA repair mechanisms
if repair fails = apoptosis via mitochondrial pathway

18
Q

O2 (superoxide anion) :
1. Production
2. Inactivation
3. Pathological effects

A
  1. Production : incomplete reduction of O2 during oxidative phosphorylation and phagocyte oxiddase in leucocytes
  2. Inactivation : by SOD
  3. Pathological effects :
    Production of degradation enzymes in leucocytes
    directly damage lipids, proteins, DNA
19
Q

H2O2 (hydroxyde perodxide) :
1. Production
2. Inactivation
3. Pathological effects

A
  1. Production : generated by SOD from O2 and by oxidase in peroxisomes
  2. Inactivation : catalase (peroxisome), glutathione peroxidase (cytosol, mito)
  3. Pathological effects :
    Destroy microbes and cells
    Can act distant from site of production
20
Q

OH (hydroxyl radical) :
1. Production
2. Inactivation
3. Pathological effects

A
  1. Production : generated by hydrolysis (radiation) and by Fenton reaction
  2. Inactivation : glutathione peroxidase
  3. Pathological effects : most reactive ROS
    damage lipids, proteins, DNA
21
Q

ONOO- (peroxynitrite) :
1. Production
2. Inactivation
3. Pathological effects

A
  1. Production : NO synthase in many cell types
  2. Inactivation : peroxiredoxins (cytosol, mito)
  3. Pathological effects :
    damage lipids, proteins, DNA
22
Q

Different type of SOD and their localisation

A

Manganese-SOD = mitochondria
Copper-zinc-SOD = cytoplasm

23
Q

Pathological effects of ROS

A

Lipid peroxidation in membranes
Oxidative modification of proteins
Lesions in DNA
Trigger necrosis, apoptosis

24
Q

Hypoxia vs ischemia

A

Hypxia = anaerobic glycolysis continue, bloodflow maintained
Ischemia = reduced flow = baisse glycolysis = more severe and rapid damage

25
Q

What is the protective response in hypoxic stress?

A

Induction of transcription factor (HIF1) = promotes angiogenesis (VEGF) = stimulates cell survival, enhance glycolysis

26
Q

How can hypothermia help in ischemic brain/spinal injury?

A

Reduces metabolic demand of stressed cells
Decrease swelling
Suppression of ROS
Inhibits inflamm response

27
Q
A
28
Q

Mechanism of reperfusion injury

A
  1. oxydative stress
  2. Ca2+ overload
  3. Inflammation (neutrophils influx)
  4. Complement activation (IgM deposit in ischemic tissu)
29
Q

Mechanisms of hypertrophy

A
  1. Mechanical sensors detect increase workload
  2. Activate downstream signal -> PI3K/AKT and GPCR pathways
  3. stimule increase production of growth factor (TGFB, IGF1) and vasoactive agents (a-adrenergic agonists, endothelin-1, angiotensin II)
  4. Actovate transcription factors (GATA4, NFAT, MEF2) = increase gene expression that encodes muscle proteins
30
Q

Mechanism of atrophy

A
  • Decrease protein synthesis
  • Increase protein degradation (ubiquitin-proteasome pathway = target cell for proteasome)
  • Autophagic vacuole = residual bodies = lipofuscine granules
31
Q

Is metaplasia a change in phenotype?

A

NON

32
Q

4 mechanisms leading to intracellular accumulations

A
  1. Inadequate removal (defect in package, transport)
  2. Accumulation of endogenous substance (defect in folding, transport)
  3. Failure to degrade (enzyme deficiencies)
  4. Depostion of abnormal exogenous substance (no enzyme activity to degrade or transport)
33
Q

What is Niemann-Pick disease?

A

Lysosomal storage dz caused by mutations affecting enzyme involved in cholesterol trafficking = accumulation

34
Q

Mechanisms in protein accumulation

A
  1. Renal reabsorption (by pinocytosis, reversible)
  2. Excessive production = Russel bodies
  3. Defective IC transport and secretion
    a) A1-antitrypsin deficiency = slow folding of proteins = partially folded aggregats in ER of hepatocytes
  4. Accumulation of cytoskeletal proteins
  5. Aggregat of abnormal proteins (amyloidosis)
35
Q

What does an accumulation of lipofuscine indicate?

A

Free radical injury

36
Q

How is melanin formed?

A

When enzyme tyrosinase catalyze the oxidation of tyrosine to dihydroxyphenylalanine

37
Q

Etiology of metastatic calcification

A
  1. increase secretion of PTH with bone resorption
  2. resorption of bone tissue (tumors)
  3. vitD disorders
  4. renal failure = retention P = hyperparathyroidisme secondaire
    Predisposed accumulation in alkaline compartiment
38
Q

Role of telomere

A

Ensure replication and protect from fusion and degradation

39
Q

What mechanisms counteract cellular aging?

A

Baisse insulin/IGF signaling, baisse TOR, altered sirtuins -> altered transcription -> increase DNA repair and protein hemostasis

40
Q

Insulin/IGF-1 signaling pathway

A

produced in response to growth hormones by pituitary gland
IGF1 = informs availability of glucose = promote anabolic state, growth and replication
downstream target = AKT, mTOR

41
Q

Mechanism of sirtuins (NAD-dependant protein deacetylase)

A

promote expressio of several genes increasing longevity (inhibe metabolic activity, reduce apoptosis, stimule prots folding, conteract ROS)
increase insulin sensitivity and glucose metabolism

42
Q
A

Nutrition (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions