Mitochondria II Flashcards
_______ is a major source of ATP in animal cells
The ATP synthesis from ADP and Pi coupled to electron transfer from NADH
ATP synthase is located in the _______ consists of _______
- inner membrane
- 2 main parts F1 and F0
the synthesis of ATP
using ATP synthase, a proton gradient and electric potential directly make ATP
F1 and F0
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
how many protons are needed to generate 1 ATP molecule
3
ATP is transported out of the mitochondria via
ATP-ADP antiporter
cell damage induces _______ of the outer mitochondria membrane, leading to _______ release
- Bak/Bax-dependent permeabilization
- cytochrome c
cytochrome c binds to several cytoplasmic proteins forming
protein complex called n apoptosome
the apoptosome activates ______, this initiating
- cascases
- apoptosis
during ischemic injury, mito also promotes ______, resulting in ______, resulting in ______
- necrotic cell death
- MPTP-dependent permeabilization of the inner and outer mitochondria membranes
- cytochrome release and elimination of the H+ gradient
lack of protein gradient blocks ______ and lack of H+ gradient causes _______
- ATP production
- ATP synthase to be converted to ATPase (thus using up all available ATP)
damaged mitochondria generates _______, causing ______
- excessive amounts of reactive oxygen
- cell damage and senescence by oxidating various other cellular proteins, lipids and DNA
what are responsible for recognizing and degrading misfolded proteins?
-mitochondrial proteases such as mAAA, iAAA and Lon
damaged mito can be “fixed” by ______ or eliminated by _______
- fusing with health mito
- mitophagy
if mito damage is extensive
mitochondira induces apoptotic cell death
accumulation of mito damage and increase in ROS is related by
senescence and increased sensitivity to neuronal degeneration
mutations in mito fusion machinery causes
autosomal dominant optic atrophy (OPA1 gene) and C-M-T neuropathy type 2A (Mfn2 gene)
mutation in mAAA protease causes
hereditary spastic paralegia
very potent toxin arsenic works by
inhibiting ox phosphorylation and inhibiting ATP production
