Module 3 Flashcards
(23 cards)
1
Q
What are mitochondria involved in
A
- hormone synthesis
- metabolism
- protein synthesis
- apoptosis
- ROS production
- Ca regulation
- pH balance
- Redox
- heat production
- neuromediator clearance
2
Q
Origin of mitochondria
A
endosymbiosis theory
3
Q
Components of mitochondria
A
- outer membrane
- inner membrane
- cristae
- inter-membrane space
- matrix
4
Q
Aerobic vs anaerobic tissue mitochondria appearance
A
- aerobic = more cristae = more ATP
- anaerobic = less cristae
5
Q
Dynamics of mitochondria
A
- form dynamic networks
- undergo fusion and fission events
6
Q
Mitochondrial fusion
A
- involved in the generation of interconnected mitochondria
- metabolically active
- mixes and unifies the metabolic compartment
- important in the dissipation of metabolic energy
- important for the completion of mtDNA
7
Q
Mitochondrial fission
A
- generation of mitochondrial fragments
- generates morphologically and functionally distinct organelles
- required for portioning of organelles during cell division, release of pro-apoptotic factors and mitophagy
8
Q
Methods of mitochondrial removal
A
- lysosomal degradation
- exocytosis
9
Q
mtDNA
A
- circular with heavy and light
- 37 genes
- inherited from mother (less error prone)
- spontaneous mutations can affect a cell but can be quickly silenced at the organism level
10
Q
Cristae in Oxidative phosphorylation
A
- shape enhances ATP production
- proton tunnelling = fewer protons needed to have a high proton conc for pumping
11
Q
What creates cristae shape
A
- ATP synthase
- OPA1
- MICOS
12
Q
What is cristae swelling mediated by
A
- heat
- pH
- osmolarity
- oxidative stress
13
Q
Metabolic syndrome and mitochondrial dysfunction
A
- Dysfunction occurs due to a reduction in SIRT-1, PPARy and PGC-1a
- Decreased mitophagy due to impairment of PINK1 pathway = accumulation of dysfunctional mito
- altered B-oxidation, decreased fusion and enhanced ROS production
14
Q
Solutions to mitochondrial dysfunction with metabolic syndrome
A
- mediterranean diet = increased SIRT-1 + PGC-1a = decreased oxidative stress and increased biogenesis
- MitoQ = antioxidant = decreases oxidative damage
- Vitamins = antioxidants
15
Q
Mitochondria and exercise
A
- immediate energy for exercise is the phosphocreatine system = DOESNT USE MITO
- short = glycolysis
- long = FA metabolism and O2 uptake
- exercise increased mitochondria turnover and cristae density = increased ATP production
- elevated MOTS-C
16
Q
MOTS-C in exercise
A
- elevated in the blood during exercise
- inhibits folate cycle = purine synthesis = AMPK activation = increased uptake of glucose = prevents insulin resistance
17
Q
Mitochondria in neuronal disease
A
- brain is dependent on mitochondrial energy metabolism and is sensitive to oxidants
- implicated in AD, PD, depression, MS, MND and epilepsy
- inactivation of fission and fusion
18
Q
Mitochondria in MND
A
- genetic mutations in SOD1, TDP43
- sporadic mutations in TDP43
- TD43 =impacts anterograde transport of mitochondria in neurones and impacts complex I =more ROS = more aggregates
19
Q
Mitochondria dysfunction in cancer
A
- cancer cells rely on anaerobic metabolism = warburg effect
- cancer cells have elevated TMAO = stable proteins
- HIF1a hypoxic effect
- cancer cells can take healthy mt from other cells via nanotubes
20
Q
Mitochondrial dysfunction in IRI
A
- Complex 1 inactivated and oxidative sites are exposed via sulfonation of cysteine residues and conformational change
- oxidative phosphorylation is impaired = decreased ATP
- accumulation of succination = binding of e- to oxygen causing reverse electron transport = ROS production
- Decreased ATP = decreased ATPase function = imbalanced NA/K+ = Ca2+ influx = ROS production
- ROS production = MPTP open = release of pro-apoptotic factors = apoptosis
21
Q
Mitochondrial transplantation to prevent IRI
A
- biopsy from pectoralis major
- isolate mitochondria
- inject healthy mitochondria
22
Q
Mitochondrial function in ischemic livers
A
- No oxygen = no final electron acceptor = accumulation of NADH and succinate
- Accumulation causes membrane potential crash as NADH and succinate release energy when donating to complexes
- ATP synthase reverses using remaining ATP to save membrane potential = ATP depletion
23
Q
Mitochondrial cristae fragmentation leading to muscle weakness
A
- Reduced SA for ETC complexes = limited proton gradient = limited ATP synthesis = restricted muscle contraction
- fragmented cristae = electron leakage = ROS production = release of apoptotic factors = activation of caspases = apoptosis
- dysfunctional organelles accumulate = toxicity
