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KIN 406 - Midterm 2
Terms in this set (159)
- what are the 2 components of it
- what does it accomplish (2)
- what is it dependent on (3)
Cell renewal and reproduction
Essential to generate and maintain complex tissue architecture
Dependent on relationships between cell proliferation, differentiation and death
2 kinds of extracellular signals for cell proliferation
What are the 4 general steps of extracellular signalling
1. Receptor-Ligand binding
2. Signal transduction
3. Cellular response
4. Change in gene expression
How do steroids work as growth factors?
Ex. testosterone, estrogen, cortisol
Penetrate cell membrane and bind to steroid receptors directly, affecting genomic regulatory mechanism
Polypeptide Growth Factors mechanism and examples
Ex. IGF-1, IGF, 2
can't penetrate membrane
acts on membrane receptors to activate kinases and start intracellular cascades
What part of the cycle are cells typical in
What happens intracellularly when cells are activated by growth factors? (7)
1. Bind to receptor
2. Activate MAPK
3. MAPK inhibits Foxo1
4. no FOXO means no p21
5. no p21 means that cyclin-cdk complexes are active
6. Complexes phosphorylate proteins that stimulate cell cycle genes
- growth factors binding to receptors also up regulates moD and myf5, stimulating cell cycle
What regulates cyclin-cdk complexes? (2)
Tumour suppressor genes
What 3 things stimulate cell growth? What 2 things inhibit it?
1. growth factor
1. tumour supressor gene
2. cdk inhibitor
What are the 5 ways the cell influence proteins to alter signalling?
1. upregulate / down regulate transcription
2. degrade protein at diff rate
3. change chemical structure slightly (phosphorylate)
4. change where it is in the cell
5. change activate state
How can change the chemical structure slightly to influence cell signalling?
You can activate / inactivate a protein.
This can be done by:
- changing the activation state (via enzymes)
- post translational modification (phosphorylation, glycosylation, or oxidation)
What is the hay flick limit? Why does it happen?
The finite # of cellular divisions in cultured cells
RNA primer is at the beginning of the DNA strand and DNA polymerase only moves in one direction. Therefore each daughter is shortened by a little bit
What are telomeres for?
Caps of junk DNA on the chromosome ends
1000-1700 bp double strand
single strand overhanging at the 3' end
compensates for shortening
Telomere Terminal Transferase (Telomerase)
Adds BP to telomeres
Low - v.low activity in adult cells
Can lead to cancerous cells
What does telomere length indicate?
Varies between cell types
Long telomere = replicate faster = leucocyte
Short telomere = replicate slower = skin fibroblast
Telomere length of different cell types (germ, stem, normal, cancer) over time?
Germ = won't decrease over time
Stem = decrease a little bit over time
Normal = decreases over time
Cancer = doesn't decrease
Why can't skeletal muscles divide easily? (4)
How often do they replicate?
Skeletal muscle is post-mitotic.
They can't divide due to their specialized structure
- very long
- complicated (individual blood supply, neural input, contractile protein)
- muscle loses function if it divides
Only replicates very rarely (no more than 1-2% is replaced per week in healthy people)
How does skeletal muscle maintain function / shape?
accessory cells (satellite cells)
Much easier than making new fibers
How so satellite cells increase muscle regeneration
expansion of satellite cells and myogenic stem cells
new myonuclei added to existing fibres
increases genetic potential and decreases muscular damage
Which of these cells would have the lowest telomerase?
- muscle fiber
- satellite cell
- cancer cell
- stem cell
- all are the same
It's post-mitotic, doesn't divide as much so it doesn't need telomerase
What kind of cells are satellite cells?
undifferentiated mononuclear cells
Who discovered satellite cells?
Where are SC located?
peripheral to myofibril
between plasma membrane and basement membrane
How are SC different than myonuclei? (3)
1. smaller nucleus
2. less organelle content
3. different morphology
marker specific to satellite cells.
Cells lose expression when they mature
Pax7 -/- mice had no SC and low muscle regeneration
When is desmin expressed?
only when SC are proliferating
When is myosin expressed?
only during contraction
What happens with a Paxy7 deficiency (3)
1. decreased muscle CSA
2. Still have some muscle (there are other factors during development)
3. But will have almost no growth
when do SC develop?
18 days after first muscle cells form
What happens to # SC with aging?
you use a lot of them up from birth - 2 months to form muscle
Difference between SC in fast and slow muscle (1 + example of a slow and fast muscle)
Fast has less SC, slow has more SC
5-12 SC per fast fiber (300 myonuclei)
30 SC per slow fiber (450 myonuclei)
Fast = EDL muscle
Slow = soleus muscle. more wear and tear, increases nuclei number
Why do fast and slow muscle have different SC?
may be due to different recruitment patterns.
More SC in muscle close to capillaries
These cells get more exposure to circulating growth factors
What is the muscle regenerative process? (8)
2. SC activated within 6 hours
3. enter cell cycle and proliferate (2-3 days)
4. form a pool of precursor cells
5. exit the cell cycle and migrate to the muscle site
6. terminally differentiate
7. can either: fuse to existing myofibril
7b. or in severe disease states they can fuse together to form new myofibril
What does the severity of injury influence in muscle?
magnitude of regeneration
Is SC activation restricted to site of damage?
Damage at one end can activate whole fiber
What are the 2 ways SC can undergo division?
1. Planar Division
2. Apical-Basal division
Describe planar division (5)
Both cells are in contact with basement membrane
Form 2 identical self cells
Form 2 SC
92% sym vs. 8% asym
Describe apical-basal division
1 cell in contact with basement membrane
1 SC and 1 myotube
18% sym and 82% asym
3 types of SC growth factors?
Things that SC growth factors might do (4)
What are the 5 categories of growth factors for SC? Which is the most important?
What are the 4 autocrine growth factors for SC?
1. IGF-1, IGF-2
What are the 5 vasculature growth factors for SC?
1. IGF-1, IGF-2
What are the 6 immune growth factors for SC?
What are the 2 motor neuron growth factors for SC?
2. neurotrophic factors
What are the 2 other growth factors for SC?
2. nitric oxide
upregulation of the following set of internal cellular factors would help promote SC differentiation?
- myf5, moD, cyclin E
- p21, myogenin, MRF4
- cyclin E, moD, MRF-4
- p21, IGF-1, MAPK
- all of the above
p21, myogenin, MRF4
IGF and cyclins both don't count because they're extracellular.
Difference between SC pre and post activation
- does not express markers associated with myogenic potential and differentiation
- SC enters cell cycle
- start expressing moD, myogenin, myf5, design, MHC
Morphological characteristics of SC (2)
large part is nucleus
Nucleus is inactive so it looks different than myonuclei
What happens during activation? (4)
1. adhesion molecules upreg
2. increased activity of cyclin-cdk complexes
3. decrease in myoD, increase in myf5
- cycles between myoD and myf5
4. allows cell cycle. Promote proliferation and inhibit differentiation
What happens during low growth factor conditions? (5)
1. low GF conditions
2. activates TF-FOXO1
3. FOXO1 activates p21
4. p21 inhibits cyclin-E & cdk2
5. allows cell cycle to go into G1
What happens when a proliferation growth factor is present? (8)
1. growth factor (like IGF-1) binds to receptor)
2. activate MAPK
3. MAPK inhibits FOXO1
4. FOXO1 makes no p21
5. This allows cyclin-E and cdk
6. This allows cell cycle
7. GF upreg moD and myf5
8. this allows cell cycle and proliferation
Satellite cell differentiation
SC withdraw from cell cycle to self renew or differentiate
4 - 5 days following injury
What happens during SC differentiation (4)
1. downreg Pax7
2. exit cell cycle
3. terminal differentiation
4. many cyclins and cdks that reg proliferation are downreg.
Experiment about SC differentiation
Gave cultured muscle tissue FBS or adult cow serum
FBS = conducive to proliferation
adult cow serum = factors for differentiation
What causes SC differentiation? (3)
Change in GF levels
Change in GF types
Change in intracellular factors that regulate proliferation and differentiation
What happens when there is a differentiation GF present? (6)
1. GF binds to receptors
2. PI3K increases
3 .PI3K activates p21
4. p21 stops cyclinE&cdk which stops cell cycle
5. PI3K also up regulates myoD, myogenin, MRF4
6. promote SC differentation
Why do levels of myoD and myf5 fluctuate during SC proliferation and differentiation?
they each do different things
MyoD = differentiation
Myf5 = proliferation
growth differentiation factor - 8
cytokine that inhibits SC prolif and differentiation
Similar to TGF-B
how does myostatin work?
inhibits myoD --> no differentiation
up regulates p21 --> inhibits cdk --> no proliferation
at days 7 - 10
becomes incorporated into existing fibres
What do terminally differentiated myocytes express (4)
SC time course following injury
Activation: 0.5 - 1
Proliferation: 1 - 5
Differentiation: 2 - 13
Maturation: 7 - 14
SC gene expression during different stages after injury
cdk34, pax3/7, sox8 - from quiescent to proliferation
myf5/6, myoD - activation to differentiation
des, myoG - proliferation to differentiation
What happens to SC with aging
Lose ends of chromosomes
Decrease in number --> less muscle region
remaining SC form worse myotubes - thin and more fragile
Population doubling limit decreases with age
Increasing non dividing SC
Population Doubling Limit
How many times cell can double in culture
6 differences between young and old isolated SC
1. young have more FOXO1 and p27
2. young have more differentiation
3. they make more myotubes
4. they make larger myotubes
5. there are more reactive to stimulus
6. they are better at fusing
What does FOXO1 do?
ultimately stops cell cycle from proliferating
What does p21 do?
inhibits cyclin E/cdk2
ultimately stops cell cycle from proliferating
What does cyclin-e / cdk2 do?
when activated they promote cell cycle
What happens to SC in people with MD
they have more muscle regeneration than normal
run through pool of SC really quickly
Deplete pool --> reduced ability to maintain muscle
Difference in telomere length of SC between healthy person and person with DMD
- barely any loss
- 13bp per year
- lose 164 bp per year
What happens to SC with disuse (5+takeaway)
1. decrease in desmin+ cells
2. decrease mRNA expression of several genes (M-cadherin, myf5)
3. less SC in inactive muscle
4. SC expand more slowly
5. form fewer and smaller myotubes
Takeaway: inactivity doesn't just affect skeletal muscle fibres - it also affects SC
During MS, what is a good indicator of proliferative lifespan of SC?
how can we use muscle SC for therapies?
1. isolate and culture muscle SC
2. transplant them
3. differentiate them to make muscle
What is FACS analysis?
What are the steps (6)
identifies which cells are SC in muscle sample
1. cells in suspension are tagged with fluorescent marker specific to undifferentiated cells (Ex. a pax7 Ab)
2. Cells are in suspension and combined with a water droplet
3. cells are sent through a nozzle under pressure. They pass 1 by 1 through an electric field and get a charge
4. flow through 2 charged plates
5. plates pull cell with the right charge to its side
6. +ve charge = non stem, 0ve charge = stem
- can sort 1mil cells per second (5k pax7 cells)
What happened when SC was transplanted from healthy donor to mdx (2)
1. the mdx mice expressed dystrophin
2. increased force generation
What are 5 possible limitations for SC transplants?
1. possible host rejection - need immunosuppressants
2. invasive - hard to get people to donate tissue
3. cells don't travel well in bloodstream, you'd have to inject it at the site
4. culturing cells changes it
5. need to find the best kind of cell for proliferation
What are 3 ways we could use growth factors to stimulate SCs?
1. find GF specific to SC
2. find a good delivery system
- Ex. packaging drugs in a microball and using lasers to burst it when at right place
3. pair treatment with certain peptides/chemicals attracted to certain areas
What is one way we could alter inhibitors to influence muscle growth?
It would activate SC
What are 4 functions of mitochondria?
1. create power for cell - via Kreb's cycle
2. role in signally apoptosis
3. regulate free radical formation / cellular oxidative stress
4. encode some of their own proteins using their now genome
Why is mito in a network?
in a branched reticular network
allows for better energy flow
Is # of mito highly variable between cells?
similar morphologically between species
within a species, there's a difference between cells
More metabolically active cell = more mito
Ex. Liver = 800 per cell
Ex. Bone = 400 per cell
Ex. RBC = 0 per cell (relies on glycolysis)
how big is a mito?
similar size to bacterium
0.5um by 2.0um
6 functions of matrix
1. Kreb's cycle
2. fatty acid oxidation
3. mtDNA replication/transcription/translation
4. protein folding / degredation
5. urea cycle enzymes
6. gluconeogenic enzymes
3 functions of inner membrane
1. oxidative phosphorylation
2. metabolite transport
3. protein import/assembly/degredation
4 functions of inter-membrane space
1. electron transfer
2. redox enzymes
3. protein import
4. apoptosis factors
4 functions of outer membrane
1. protein import
2. metabolite influx/efflux
4. signalling molecules
Structure of mtDNA
located in matrix
double stranded circular DNA, like bacteria
Only 1 significant region is noncoding
< 6% noncoding (compared to 95%+ of nDNA)
contains multiple copies of a gene
more likely to have higher mutation rate
Replication of mtDNA (#)
2-10 copies of mtDNA per mitochondria
Replication not linked to cell cycle
mitochondrial biogenesis = can increase mitochondrial content in terminally differentiated cells
Inheritance of mtDNA
mtDNA copy # = 1k in sperm, 100k-1mil in eggs
sperm mtDNA gets diluted and degraded during fertilization
Which cell has highest mtDNA copy#?
b) slow skeletal muscle
c) fast skeletal muscle
d) cardiac muscle cell
Cardiac muscle = almost exclusively dependent on oxidative metabolism
RBC is all glycolytic.
Slow skeletal muscle has more mitochondrial than fast muscle
- relies more on oxidative (slow-ox) than fast which relies on glycolytic more (fast-gly / FOG)
subunits of mtDNA
2 rRNA genes
22 tRNA genes
13 genes that synthesize 13 proteins essential for oxidative phosphorylation system
- 7 subunits for NADH dehydrogenase / complex I
- 3 subunits for cytochrome c oxidase / complex IV
- 2 subunits for ATP synthase / complex V
- 1 subunit for cytochrome c reductase / complex III
permanent change in DNA
all myDNA looks the same because it has the same code.
Most people have normal mtDNA without mutation
Why does mtDNA have such a high mutation rate compared to mtDNA? (4)
1. no histone protection
2. mtDNA repair is less efficient
3. less non-coding regions
4. in matrix - leaky electrons may be reactive
What tissues have more mtDNA mutations?
highly oxidative tissues
Ex. liver, brain, heart
because these tissues depend more on ATP and depend on oxidative phosphorylation
Also post-mitotic cells because they're long lived
Ex. brain, heart, skeletal muscle
wild type and mutated genomes can co-exist.
Can have some mtDNA copies WT and some mutated
can occur within and between tissues depending on how mtDNA segregates
When cells divide, mitochondria are randomly distributed
One cell might get all the mutated or all normal
Ratio of wild type: mutant may differ between cells and tissues
The percentage of mutation determines severity
What %age of mtDNA can be mutated without showing clinical symptoms
No symptoms up to 70% mutations
At 70% you can't make enough normal proteins and you start to see symptoms
Phenotype of mtDNA
passed down maternally
but ratio of WT:mutated isn't always the name
random distribution in eggs
offspring of mother can range percentage of DNA
men and women can have mutated mtDNA
5 steps of mtDNA transplant
1. take fertilized oocyte nucleus (nDNA)
2. take donor oocyte with normal mtDNA
3. remove nucleus
4. put in other nucleus
5. now you have a zygote with 3 ppl DNA
Difference in mito content between muscle fiber types
slow = highest mito content
fast = lowest
the content is stable in most tissues
but not muscle
can increase with contractile activity / disease or can decrease with inactivity or disease
What are the 2 locations of mitochondria in muscle?
Proportions of each in muscle
What are the 6 things mito from either location differs on?
1. Subsarcolemma mito (SS) = under sarcolemma (25%)
2. intermyofibrilar mito (IMF) = between myofibrils (75%)
they have different
- proteins and membrane
- ability to make ATP
- ability to regulate ROS
- ability to signal cell death
- rate of respiration (SS has lower)
- resting [ATP] (SS has lower)
What is PGC-1?
master regulator of mitochondrial biogenesis.
Activates TF that promotes creation of mitochondria
How is PGC-1 activated?
High cytosolic Ca
AMPK activates PGC-1
activates mito biogeny
What is an issue with activating PGC-1?
AMPK is sensitive to ATP:ADP:AMP ratio
What happens in the body during energy deprivation?
1. strenuous exercise
2. ATP decreases
3. ATP --> ADP --> AMP
4. tells system that it's not good at making ATP
5. Makes more ATP to compensate
What pathway happens when someone is cold?
1. activate cAMP
2. activate PKA
3. activate CREB
4. trigger mito biogen
Why would fasting increase mitochondrial biogenesis?
The need to switch fuel sources.
Decrease in use of carbs leads to increase in use of fat / proteins
What happens to muscle when PGC-1 is over expressed
Ex. can artificially increase PGC in planteris (fast ox)
increases mitochondrial content which increases oxidative potential
goes from white --> red
why are mtDNA and mito myopathies common in skeletal muscle? (3)
1. high energy needs - easy to notice clinical symptoms
2. post mitotic tissues with little regeneration - mtDNA mutations can accumulate
3. muscle biopsy is more common than other tissue biopsies
3 ways to increase PGC-1
how many proteins are needed in the ETC? Where do they come from?
13 from mtDNA
1500 from nDNA
What can influence mitochondria to become dysfunctional (3)
bad protein import
What is happening in a fiber that has a lot of SDH but not COX?
Why aren't all fibres like that?
- some have COX
- some don't have COX but also don't have SDH overproduction
SDH = indicates there are a lot of mitochondria
no COX = part of the ETC - means that the ETC isn't working
SDH is all nDNA but COX is partially mtNDA
- this indicates mtDNA mutation
SDH overproduction is compensation for lack of ATP production
Not all fibers
- mtDNA is randomly distributed, not all with have that mutation
- some may have mutation so no COX but not have SDH overproduction because it may not be recruited as often and have less ATP needs
How do proteins encoded by nDNA get into the matrix? (4)
1. synthesized in cytosol
2. Targeted by cytosolic chaperones that lead proteins to mitochondria
- Ex. heat shock protein 70 (Hsp70)
- Ex. mitochondrial import stimulation factor (MSF)
3. TOM lets it into inermembrane space
4. TIM lets it into matrix
What is TOM and TIM?
How do they work?
What can they influence? (3)
TOM = translocases of outer mem
TIM = translocases of inner mem
they form pores at membranes, allowing precursor proteins in
level and function influence
1. mito protein import
2. mito function
3. mtDNA maintenance
Usually H+ movement to matrix is coupled to ATP formation. Sometimes H can leak across inner mem without forming ATP
UCP lead to protons leaking without forming ATP
You need more electrons / substrate.
Increases BMR by 35-45%
What happens when a mouse has high UCP
1. more O2 consumption since you're moving more electrons
2. lower resting fat stores
3. increased resistance to obesity following a high fat diet
4. heat production
Why can't a UCP pill work for weight loss? What is an alternative
because too much heat can degrade proteins
instead we can do small amounts of UCP with gene editing
Steps of fatty acid transport into the mitochondria (7)
1. Activate FA by using acyl CoA into FA-acyl CoA using acyl-CoA synthase
2. Enter cell's outer membrane using specific transporter
3. Need to change composition to cross inner membrane.
- exchange CoA to carnitine to make Fatty acyl-carnitine
- use CPTI
4. Transfer fatty acyl-carnitine into matrix using carnitine-acylcarnitune translocate
5. once in matrix, CPTII changes carnitine back to CoA to reform fatty acyl CoA
6. Fatty acyl CoA is broken down by B-oxidation into acetyl CoA units
7. carnitine transported back to inter-membrane space by carnitine-acyl carnitine translocase
Why do we have such a complicated system for getting FA into matrix? (2)
allows us to control rate of fats in mitochondria
We don't want fat to accumulate into mitochondria
What does VDAC and ANT stand for?
What do they do?
Specialized channels that regulate movement of: ATP, ADP, Ca, small proteins. Also involved in apoptotic cell death
VDAC = voltage deep anion channel
- on outer membrane
ANT = adenine nucleotide translator
- on inner membrane
What happens when there's an ANT deficiency?
ATP couldn't leave mitochondria
Proliferation of mito to compensate for lack of ATP
How does PGC-1 levels influence COX activity?
What influences PGC-1 levels?
More PGC = more COX = more ETC activity = more ATP being made
Inactivity decreases PGC
Activity increases PGC
increases PGC-1 activity
increases mito function and tissue activity
Only targets 1 protein of exercise. Exercise does so much more than that.
What happens to mitochondria in skeletal muscle with age? (4)
oxidative phosphorylation decreases
mito content decreases, thus ATP production decreases
each mitochondria also makes less ATP individually
Increase in dysfunctional mitochondria --> compensation --> increased ragged red fibres
What happens to mtDNA in skeletal muscle with age?
copy number decreases
due to decrease mito content, but also decreased copy number per mito
Do mtDNA mtuations cause aging
D257A mice have myDNA mutations and aging phenotypes
Accelerated muscle wasting
increased cell death
The function of which of the following could be affected by mtDNA mutation?
a) NADH dehydrogenase
d) A & B
e) A & B & C
d) A & B
SDH is entirely nDNA
The other 2 have subunits encoded for by mtDNA
**are we just supposed to know what things are encoded by which DNA?
What are ragged red fibers
they stain positively for trichrome stain
Accumulation of mito in the fibres.
They cluster near membrane.
due to fiber trying to compensate for lack of ATP production when the problem isn't lack of mito, it's dysfunctional mito
What were the results of the MZ twins with OP-MD study?
did mtDNA analysis
One twin has some intact DNA and some with a deletion (we know because it's smaller)
Other twin has a bunch of deletions
twins had same nDNA but different mtDNA- this influenced phenotype
influence of mtDNA on mito (3)
prevents mtDNA mutations, mito alterations and atrophy
What are Pole G Animals? (1+4)
Accelerated aging model animals.
- reduced mtDNA copy number
- more mutations in mtDNA
- reduced muscle weight
- ultilaately decreased mito function
What happens when you put pole G animals on exercise programs?
- one with exercise doesn't show aging phenotype
- copy number increases
- number of point mutations decreases
- mito look healthier
- muscle weights restored
endurance animal dies faster than WT, but slower than sedentary one
Why does exercise improve mito so much?
Exercise stimulates PGC1 which creates more mito
increased clearance of damaged mito so we can get rid of them, So we're left with healthier mito pool
pathway upreg by things like exercise and starvation
Because of need for fuel we start breaking down things in cell we don't likely need.
So it gets rid of things that are damaged.
Calorie restriction with monkeys
Reduced calorie diet showed less aging.
Fewer animals taking in fewer calories which forced them to use up other parts of body (junk proteins) as fuel source.
Similar effect with exercise
Gets oxidized itself
molecule with an unpaired electron in its orbital
They are highly reactive because they want to become stable by stealing electrons from other compounds
Reactive Oxygen Species
compounds derived from partial chemical reduction of molecular oxygen.
Reactive but not necessarily FR since they don't always have unpaired E
formed by one e- reduction of oxygen
We use oxygen at mito as final electron acceptor
Reactive but usually short lived.
When reacts with hydrogen it makes hydrogen peroxide
H202 is an ROS but not a FR
more stable than superoxide radical, but it's longer lived so it can travel.
Can pass through biological membranes
How hydrogen peroxide can convert to hydroxyl radical
Easily convertible to hydroxyl radical (OH) which is more highly reactive
Fenton Reaction: Reductive cleavage of H2O2 with transition metal
Ex. Fe2+ + H2O2 --> Fe3+ + OH + OH
Nitric Oxide (what is it, what is its role)
Nitrogen based free radical
"reactive nitrogen species" RNS
Involved as signalling molecule
Ex. promotes vasodilation of smooth muscle
forms when NO combines with superoxide
Long lived and reactive
Might explain vascular dysfunction in CVD
How is superoxide radical formed?
one electron reduction of ground state O2
how is hydroxyl radical formed?
one electron reduction of hydrogen peroxide
How is peroxynitrite formed?
reaction of nitrogen molecule with superoxide radical
2 major classes of antioxidants
Antioxidant enzymes (can upreg or downreg gene expression)
Biological / chemical antioxidant (we can't change activity, it just has to do with amount present)
3 major antioxidant enzymes
1. superoxide dimutase
3. glutathione peroxidase
How are antioxidants made?
We can make them in the body
Induced by oxidative stress
If we get a high level of FR, it signals the body to make more antioxidants
What is a function of an antioxidant?
a) prevent ROS / RNS generation
b) prevent oxidation of cellular components
c) decrease reactivity of ROS/RNS
d) B & C
e) A & B & C
d) B & C
Antioxidants will not prevent FR formation.
They are just fixing it when it already happens
They are making them less reactive, thus hopefully preventing other cellular components from being oxidized
What are the 2 forms of superoxide dimutase?
- found in cytosol
- found in matrix
- 15 - 20% of total SOC
- made in cytosol and transported into mito
- entirely nDNA
What doe SOD do?
catalyzes reaction of superoxide + H to form H2O2 + O2
Breaks down superoxide to make something less reactive
breaks down H2O2 into water and oxygen
found in mito and other organelles
2H2O2 --> 2H2O + O2
Also breaks down H202
Also found in mito and cytosol
Does so slightly differently than catalase
Brings in GSH
takes electrons from GSH to give to H202
this forms water and glutathione disulphide (GSSG)
GSSG is not very reactive
but eventually we would run out of GSH
Luckily there's a mechanism to turn GSSG back into GSH
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