electron transport chain Flashcards

1
Q

how can energy carried by the
-electrons are unlocked in cells:
the cell can harvest the energy carried by these electrons using —– which consists of series of —– in the inner mitochondria membrane which accept and pass on electrons.
- uses the energy from electron to make —– by the following formula:

A
  • electron transport chain
  • proteins
  • atp
  • adp + pi —> atp
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2
Q

1.the etc is located in the ——
2. —– and —– used to generate energy to make atp
3. outer membrane is — to small molecules
4. inner membrane is —- to most ions , small and large molecules
5. NADH , FADH2 need to reach the —– for atp sythesis
6. glycolysis takes place in the —- and tca cycle in —- ( except succinate DH which is also part of ETC complex II)

A
  • inner mitochondrial membrane
  • nadh and fadh2
  • porous
  • impermeable
  • etc complex
  • cytoplasm
  • mitochondrial matrix
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3
Q

——- are transport proteins permit passage of specific molecules from cytosine to mitochdoniral matrix

A

substrate shuttle

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4
Q

1.some NADH is generated by glycolysis in the —- but the inner mitocondrial membrane lacks an ——-
2. only electrons from —- NADH are transported in the mitochondrion by shuttle system
3. electrons from cytosolic NADH transferred to an —— which crosses the mitochondrial membrane and then transfer those electrons back to ———
4. glycerol 3 phosphate shuttle -e from —— transferred to —–
5. malate aspartate shuttle - e from —– transferred to —-

A
  • cytosol
    -NADH transport protein
  • cystolic
  • intermediate
  • mitochondrial NAD+ or FAD
  • systolic NADH
  • mitochondrial FAD
  • cystolic NADH
  • mitochondrial NAD+
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5
Q

electron transport chain component :
1. complexes —-
2. each complex can donate and accept e- to —— ( cyt C and coQ )
3. —- can receive and donate e-
4. electrons ultimately combine w — and — to form —-

A
  • I-IV
  • mobile carriers
  • carriers
  • 02 and hydrogen
  • froms h20
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6
Q

respiratory chain components ( freely diffusible components ) :

A
  • NADH ( mitochondrial matrix )
  • coenzyme Q ( ubiquionine ) ( mobile within lipid bilayer )
  • cytochrome C ( peripheral membrane protein outer membrane surface )
  • molecular 02
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7
Q

all members of the chain except coenzyme Q are — protein complexed .
they are coupled to —- which makes them very good electron carriers. eg
hydrogen carriers eg:

A
  • large
  • metal ions as: iron and iron sulfure centres , porphyrin ring ( fe iron ) or copper ions ( cytochromes )
    formula: fe+3 —-> ( +e) to from Fe+2 —-> ( -e) to from fe+3
  • FMN , FAD
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8
Q

The 3 multi-protein complexed are localised in —- and they include:

A
  • inner mitochondrial membrane
    I. NADH-Q reductase ( NADH dehydrogenase ) fe-sulphur centre for e- transport
    III. cytochrome C reductase complex: cytochrome ( fe ion ) centre for e- transport
    IV. cytochrome C oxidase: copper an cytochrome e carriers
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9
Q

—- catalzyes the transfer of e- from NADH to coQ ( ubiquitoun )

A

complex I ( NADH-ubiquinone oxireductase )

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10
Q

—– transfers e- from succinate to coQ

A

complex ii succinate ubiquinone oxidreducase or succinate dehydrogenase

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11
Q

—— transfers e- from ubiquinolol ( reduced form of ubiqionine CoQH2 or UQH2) to cytochrome c

A

complex iii (cytochrome bc1 complex ) ubiqionolul-cytochrome c reductase

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12
Q

—- transfers e from cytochrome c to 02

A

complex iv cytochrome c oxidase

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13
Q

—– is released as electrons passed from complex to complex and this energy is used to pump — across membrane
1. – sites of proton pimping when e- enter from —- so 1NADH yields to —–
2. – sites of proton pumping when e- enter from —- so 1 FADH2 yields to —-
3. electron trasport is tightly coupled to —-

A
  • free energy
  • protons (H+ )
  • 3
  • NADH
  • 3 ATPS
  • 2
  • FADH2
    -2 ATPS
  • proton pumping
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14
Q

oxidatitive phosphorylation:
- electrons from NADH FADH2 passed on to —
- — is the final acceptor of electrons
- as electrons are passed down complexed on chain — is released
- released energy is used to —- across the membrane
- —- are moved back into mitochondrial matrix through —-
- —–makes ATP from energy of H+ moving through h+ channels

A
  • electron transport chain
  • 02
  • energy
  • pumping h+
  • protons
  • ATP sythsase
  • ATp synthase
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15
Q

chemiosomotic hypothesis ( describe how ATP is generated from transport of electrons in the ETC ) :

A

1- protons are pumped from mitochondria matrix to intermemnbranous space : the site of proton pumping = 3 complexes of ETC , the inner mitochondrial membrane is impermeable to protons , thus when protons are pumped out a gradient is created ( proton motive force )
2- the proton gradient formed is used to make atp sythesis : uses h+ gradient to drive arp sythesis :
-H+ move back to the mitochondrial matrix through specific proton channel.
-Complex V: Fo unit - integral membrane protein that contains the proton channel, attached to F1 unit (ATP synthase).
-H+ passage through F0 causes rotation.
-F0 Rotation  conformational change F1 allowing binding of ADP + Pi

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16
Q

uncoupling protein is found in — an it creates , energy is released as —- ( non-shivering —– )

A
  • inner mitochondrial membrane
  • proton leak
  • heat
  • thermogenesis
17
Q

——-responsible for heat production in brown adipose tissue.

A

thermogenin ( UCP1 )

18
Q

brown fat uses —- respiratory energy for —- production in response to cold , humans have —- brown fat excepts neonates

A

90% , heat , little

19
Q

—– are compounds that increase permeability of the inner mitochondrial membrane ( e.g. 2,4-dinitrophenol & pentachlorophenol)

A

synthetic uncouplers

20
Q

synthetic uncouplers have no —- and energy is released as —-

A
  • atp sythetsis
  • heat
    ( Overdose of Aspirin & other salicylates uncouple oxidative phosphorylation leading to a fever! )
21
Q

—– are compounds that increase permeability of inner mitochondrial membrane

A

endogenous uncouplers
examples:
1.bilirubin at high concentrations
2.Bilirubin toxic to neurons and oligodendroglia
3.Bilirubin uncouples electron oxidative phosphorylation
4.can cause severe brain damage in infants.

22
Q

knrenicterus is a rare — disorder characterised by excessive levels of — in the blood during infancy if jaundice untreated

A
  • neurological
  • bilirubin ( hyperbiluribenamiea)
23
Q

mitochondrial diseases:

A

OXPHOS diseases
Defects in oxidative phosphorylation as a result of mutations in genes encoding various complexes of ETC
Inherited or de novo mutations in either nuclear DNA or mtDNA
Impaired oxidative phosphorylation in:
Parkinson’s
Alzheimer
Cardiomyopathies
Affects tissues with highest energy demand: heart, muscle, nervous tissue & kidney
Examples of affected genes: ATP synthase or mitochondrial tRNA

24
Q

mitochondrial diseases:

A

Leber hereditary optic neuropathy

Point mutations in one of the subunits for NADH-Q reductase, QH2 (I), cytochrome c reductase (III) or cytochrome oxidase (IV).
Sudden onset of blindness in young adults.

Result:
Impaired e- flow through respiratory chain & ATP synthesis.

Optic nerve has high energy demand & relies almost entirely on oxidative phosphorylation.

25
Q

inhibition of the etc leads to inhibition of — and cell —

A
  • atp sythesis and cell death
    (
    Riboflavin deficiency affects Complex 1 and 2 (Flavin is a component of FMN, FAD)

Rotenone (poison) inhibits at Complex I.

Doxorubicin inhibits at CoQ.

Fe deficiency inhibits any of the Fe-containing complexes.

Cn- and CO inhibit Complex IV – compete with O2 for binding. )

26
Q

vitamine déficiences:

A

Coenzymes:
NAD  Niacin (B3)
FAD  Riboflavin (B2)

Symptoms:
Severe lethargy & fatigue
Complications affecting the cardiovascular, nervous, muscular, & gastrointestinal systems.