Mitochondria II Flashcards

1
Q

_______ is a major source of ATP in animal cells

A

The ATP synthesis from ADP and Pi coupled to electron transfer from NADH

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2
Q

ATP synthase is located in the _______ consists of _______

A
  • inner membrane

- 2 main parts F1 and F0

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3
Q

the synthesis of ATP

A

using ATP synthase, a proton gradient and electric potential directly make ATP

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4
Q

F1 and F0

A

spans the inner mitochondira membrane and form a proton channel. F1 is bound to F0. F0 uses the energy of the H+ movement through the channel to generate ATP

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5
Q

how many protons are needed to generate 1 ATP molecule

A

3

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6
Q

ATP is transported out of the mitochondria via

A

ATP-ADP antiporter

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7
Q

cell damage induces _______ of the outer mitochondria membrane, leading to _______ release

A
  • Bak/Bax-dependent permeabilization

- cytochrome c

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8
Q

cytochrome c binds to several cytoplasmic proteins forming

A

protein complex called n apoptosome

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9
Q

the apoptosome activates ______, this initiating

A
  • cascases

- apoptosis

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10
Q

during ischemic injury, mito also promotes ______, resulting in ______, resulting in ______

A
  • necrotic cell death
  • MPTP-dependent permeabilization of the inner and outer mitochondria membranes
  • cytochrome release and elimination of the H+ gradient
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11
Q

lack of protein gradient blocks ______ and lack of H+ gradient causes _______

A
  • ATP production

- ATP synthase to be converted to ATPase (thus using up all available ATP)

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12
Q

damaged mitochondria generates _______, causing ______

A
  • excessive amounts of reactive oxygen

- cell damage and senescence by oxidating various other cellular proteins, lipids and DNA

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13
Q

what are responsible for recognizing and degrading misfolded proteins?

A

-mitochondrial proteases such as mAAA, iAAA and Lon

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14
Q

damaged mito can be “fixed” by ______ or eliminated by _______

A
  • fusing with health mito

- mitophagy

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15
Q

if mito damage is extensive

A

mitochondira induces apoptotic cell death

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16
Q

accumulation of mito damage and increase in ROS is related by

A

senescence and increased sensitivity to neuronal degeneration

17
Q

mutations in mito fusion machinery causes

A

autosomal dominant optic atrophy (OPA1 gene) and C-M-T neuropathy type 2A (Mfn2 gene)

18
Q

mutation in mAAA protease causes

A

hereditary spastic paralegia

19
Q

very potent toxin arsenic works by

A

inhibiting ox phosphorylation and inhibiting ATP production