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Functions of mitochondria
ATP production
apoptosis
non-shivering thermogenesis
storage of calcium
building various structures
what is the 1st example of another function of mitochondria
assist with synthesizing, breaking-down and recycling biochemicals for cell function
what is the 2nd example of another function of mitochondria
assist with synthesis of blood components and certain hormones
what is the 3rd example of another function of mitochondria
role in cholesterol metabolism
what is the 4th example of another function of mitochondria
cell differentiation, signalling and controll over cell cycle and cell growth
2 ways of how ATP is made
substrate level and electron transport
substrate-level phosphorylation
substrate - p (adp) = intermediate + ATP
electron transport phosphorylation
protons flow because of chemiosmotic gradient
flow through a special channel protein
oxidative phosphorylation complex 1
NADH dehydrogenase
oxidative phosphorylation complex 2
succinate dehydrogenase
oxidative phosphorylation complex 3
cytochrome c reductase
oxidative phosphorylation complex 4
cytochrome c oxidase
end of mitochondrial intermembrane space
ATP synthase
what are electrons transported through in oxidative phosphorylation
a chain of protein complexes that
what does NADH do in the beginning oxidative phosphorylation
gives off electrons to move through the chain
what are the internal structures of PC1
FMN
series of iron-centers
iron-sulphur center
what happens at protein complex 1
NADH oxidized to NAD+
2 electrons to FMN
electrons through iron centers
stop at iron sulphur center
creates proton gradient for 2H+
reduces ubiquinone to ubiquinol
what is the result of the flow of electrons in PC1
4H+ into inter-membrane space
where does ubiquinol go from protein complex 1
to protein complex 3
internal structures of protein complex 3
cytochrome B
rieske iron sulphur proteins
cytochrome c1
cytochrome c1
mobile protein moving in intermembrane space
what happens at protein complex 3
2 electrons off to cytochrome c
travel through intermembrane space
bind to protein complex 4
what is the result of the flow of electrons in PC3
gives enough energy to pump 4H+ into intermembrane space
what happens to cytochrome C
it binds one of the subunits of protein complex 4
how many subunits does complex 4 have
3
what happens after cytochrome C is bound to complex 4
2 electrons are given off to complex 4
what does complex 4 do to oxygen
reduces it to H2O molecule
what happens at the same time as complex 4's interaction with oxygen
the electrons given off pump 2H+ ions inton intermembrane space
how many H+ ions does 1 NADH pump into the intermembrane space
10
how do H+ ions make ATP
they move down the ATP synthase
how many H+ ions need to move through synthase to make 1 ATP
4
ATP synthase complexes
F0 and F1
F1 complex
has alpha and beta subunit
what happens as H+ ions move through F0 complex
subunits rotate
phosphorylate ADP to ATP
using an inorganic phosphate and ADP in matrix
when is FAD reduced to FADH2
during the krebs cycle when succinate is oxidized to fumarate by succinate dehydrogenase
how many subunits does protein complex 2 have
4: a, b, c, d
what is in the center of protein complex 2
iron centers
what happens at protein complex 2 of FADH2 pathway
2 electrons pass through iron centres to ubiquinone
ubiquinone reduced to ubiquinol
ubiquinol moves to protein complex 3
what happens from the protein complex 3 point of the FADH pathway
flow of electrons and processes are the same as the NADH pathway
Malate aspartate shuttle: aspartate aminotransferase
catalyzes conversion of alpha-ketoglutarate and L-aspartate to glutamate and oxaloacetate
Malate aspartate shuttle: malate dehydrogenase
oxidizes NADH from glycolysis in the cytoplasm to NAD+ while oxaloacetate is reduced to malate
oxidizes malate in mitochondria to oxaloacetate
what happens when malate dehydrogenase oxidizes malate
NAD+ reduced to NADH
oxidized in the ETC to make 2.5 ATP
glycerol-phosphate shuttle step 1
DHAP reduced to G3P
NADH ox to NAD+
catalyzed by G3PDH
glycerol-phosphate shuttle step 2
G3P moves freely into MT
ox to DHAP by G3PDH
in oxidative phosphorylation: phosphorylation is tightly coupled to what
electron transport under most circumstances
electrons do not usually flow through ETC to oxygen unless what
ADP is phosphorylated to ATP
oxidative phosphorylation requires what
substrates, ADP, Pi, O2
ADP most important
level of ADP determines what
rate of oxidative phosphorylation
what happens if ADP is added to oxidative phosphorylation
rate of O2 consumption increase
what happens as ATP is formed from ADP
rate of O2 consumed slows down
what happens to oxidative phosphorylation in the absence of ADP
electron flow stops
O2 not consumed
no ATP made
what happens to oxidative phosphorylation in the absence of O2
electron flow stops
ADP not consumed
no ATP made
what is oxygen consumption is linked to what
ATP production
how does coupling occur
indirectly via H+ electrochemical gradient
any blocking in the ETC causes what
prevention of phosphorylation
any blocking of phosphorylation causes what
stops electron transport
any blocking in the ETS causes what
prevention of oxidative phosphorylation
when does inhibition happen
when we ingest specific amounts of specific substances/poisons that block enzymatic activity in ETC
adding synthetic substances for scientific experiments
what disrupts coupling of electron transport and phosphorylation
uncouplers
what is the effect of uncouplers
ATP not formed
PMF across inner mitochondrial membrane dissipated
why do protons in intermembrane space cross the inner mitochondrial membrane without interacting with ATP synthase
due to proton leak, uncoupling protein or agent acting as proton carrier
during uncoupling what happens to protons once in the matrix
they still bind with oxygen to form water
what happens to all energy contributed in uncoupling
it is lost as heat while on outside of proton gradient
how does the ETC attempt to rectify decrease in proton gradient
speeding up the ETC and increasing O2 consumption
what is the result of ETC rectifying the decrease in proton gradient
more NAD+ is produced increasing the krebs cycle as well as CO2 production
this increases respiratory rate and BMR
tightly coupled
no electron flow without phosphorylation and vice versa
partially uncoupled state
normal mitochondrial function under physiological condition due to proton leak and uncoupling proteins
makes necessary heat
dys-coupled respiration
occurs under pathological and toxicological conditions
results in mitochondrial dysfunction
uncoupled respiration
experimentally induced
apply uncouplers
obtain reference state for evaluation of respiratory capacity
regulated uncoupling
generates heat to maintain body temperature
in what does regulated uncoupling occur
hibernating animals
newborns
mammals adapted to cold
example of regulated uncoupling
cold exposure
SNS secretion of norepinephrine
norephinephrine binds to beta-3-adrenergic receptor
activates adenylate cyclase
activate camp levels
camp levels activate PKA
PKA activates triacylglycerol lipase
converts triacylglycerol to FFA
FFA activate UCP1
DNP
lipid soluble
weak acid
H+ carrier
provide pathway for flow of H+ across inner mitochondrial membrane
bypass ATP synthase
what happens when DNP is added to a cell
stops ATP synthesis
doesn't block oxygen uptake
electron transport and H+ pumping continue rapidly
no H+ gradient
when does uncoupling take place
protons enter matrix of mitochondria by bypassing ATP synthase
causes decrease in electrochemical proton gradient
necrosis
not planned
insult to cell causing damage
chemical or mechanical
cells swell, explode and release contents
damage other cells
inflammation
apoptosis
programmed cell death
neat and structured
necessary for normal development
destroy harmful agents
apoptotic blood system
produce and replace old blood cells with new ones
how does apoptosis terminate immune response
kills t-cells to prevent them from killing healthy cells
intrinsic apoptosis
cell damage
BAX released
attaches to prevent Bcl-2 from inhibiting apoptosis
cytochrome-c binds apaf 2
forms apoptosome
activates caspase 9
extrinsic apoptosis
starts outside cell
death receptors bind death activators
activates caspase 8
destroys organelles, structures and DNA of cell
AIF apoptosis
doesn't include caspase
located in intermembrane space of mitochondria
cell damaged
AIF released into cytoplasm
moves into nucleus to bind DNA of cell
destroys DNA
activates apoptosis in neurons
calcium functions
activate enzymes
component in blood clotting cascade
intercellular signal
intercellular signals of calcium
relax and constrict blood vessels
cell aggregation and movement
muscle protein degradation, muscle contraction
secrete hormones
cell division
nerve impulse transmission
calcium in mitochondria
regulates organelle metabolism
trigger or prevent apoptosis
buffers and shapes cytosol calcium signalling
why are calcium ion levels in cytoplasm very low
calcium ions will bind proteins in cytoplasm
conformational change that exposes hydrophobic components to aqueous environment
calcium protein complexes insoluble
MICU 1 and 2
special proteins that inhibit MCU at low concentrations
at high concentrations Ca2+ bind EF hands of both
deactivates MICU2 and MICU1 activates MCU
