Mitochondrion Function

Question 1

Describe the role mitochondria play in cellular metabolism

Answer 1

Produce ATP via oxidative phosphorylation
Regulate metabolic pathways
Calcium homeostasis
Programmed cell death - apoptosis
ROS Production and Detoxification
Stem cell regulation

Question 2

Explain the role mitochondria play in cellular respiration

Answer 2

ATP production - provides energy for cellular processes
Enable cells to use oxygen efficiently for energy production
CO2 production
House the machinery for both the citric acid cycle and oxidative phosphorylation, where most of the energy from nutrients is extracted and converted into a usable form for the cell

Question 3

Identify mitochondria as a major source of reactive oxygen species (ROS

Question 4

Describe glycolysis:

Answer 4

Glycolysis occurs in the cytoplasm outside of mitochondria
1 molecule of glucose is phosphorylated into 2 pyruvate molecules
Energy investment phase - Two molecules of ATP are used to phosphorylate glucose and prepare it for breakdown
Energy payoff phase - Four molecules of ATP and two molecules of NADH (an electron carrier) are produced, resulting in a net gain of 2 ATP per glucose molecule.

Overall products;
2x Pyruvate (3 Carbon)
2x ATP (net gain)
2x NADH

Question 5

Describe the Kreb’s cycle:

Answer 5

Series of enzyme-catalyzed chemical reactions that take place in the mitochondrial matrix
Acetyl CoA broken down
Overall products per acetyl CoA;
2 CO₂
3 NADH (electron carrier),
1 FADH₂ (electron carrier),
1 ATP (or GTP) (energy).
NADH and FADH₂ produced carry electrons to the electron transport chain for ATP production through oxidative phosphorylation

Question 6

Give a summary of oxidative phosphorylation:

Answer 6

Occurs in the inner mitochondrial membrane
Electrons from NADH and FADH₂ (produced in the Krebs cycle) are transferred through a series of protein complexes in the electron transport chain
As electrons move through the chain, energy is released, which pumps H⁺ ions from the mitochondrial matrix into the inter-membrane space, creating a proton gradient
Chemiosmosis - proton gradient drives protons back into the matrix through the enzyme ATP synthase, which uses this flow to synthesise ATP from ADP and inorganic phosphate
Oxygen acts as final acceptor, combines with e- and H+ to form water
Around 34 ATP molecules are produced per glucose molecule

Question 7

Describe Complex I in ETC:

Answer 7

NADH dehydrogenase complex
Transfers electrons from NADH to ubiquinone (Q)
Transfers protons from mitochondrial matrix
to intermembrane space
Results in reduction of U and oxidation of NADH

Question 8

Describe Complex II in ETC:

Answer 8

Cytochrome b-c1 complex/ Q
Transfers electrons from succinate to ubiquinone
Results in reduction of U and oxidation of NADH

Question 9

Describe Complex III in ETC:

Answer 9

Cytochrome oxidase complex
Transfers electrons from QH2 to 2 cytochrome c molecules
This oxidises Q and reduces cytochrome c
Transfers protons from matrix to
intermembrane space

Question 10

Describe Complex IV in ETC:

Answer 10

Cytochrome c oxidase
Transfers electrons from cytochrome c to O2
This oxidises cytochrome c and reduces O2
Uses protons from the matrix side of the membrane to form H2O
Transfers protons from matrix to inter-membrane space

Question 11

Describe Complex V in ETC:

Answer 11

ATP Synthase
Enzyme complex that catalyses the final stage in oxidative phosphorylation
ATP is generated from ADP and Pi
A molecular machine – a turbine driven by protons flowing through
the transmembrane protein
complex, across the inner
mitochondrial membrane

Question 12

Describe lipid metabolism:

Question 13

What are antioxidants and how do they prevent free radical damage ?

Answer 13

Substance that when
present in low concentrations (compared to that
of an oxidizable substrate) will significantly
delay or inhibit the oxidation of that substrate
Antioxidants prevent free radical damage by:
* preventing the formation of radicals
* scavenging free radicals
* promoting their decomposition

Question 14

Explain mitochondria as a source of ROS ?

Answer 14

Mitochondria produce Reactive Oxygen Species in the electron transport chain.
Some e- leak out of ETC before reaching last electron acceptor and instead combine with O2 to form superoxide anion O₂−
Superoxide anion is a free radical
Complex I releases O2- into matrix
Complex III can release O2 *- into matrix & inter-membrane space

Question 15

What is a free radical ?

Answer 15

A free radical is any atom with at least one unpaired electron in the outermost shell
A free radical will tend to ‘steal’ electrons from other atoms which generates a new free radical and establishes a chain reaction
Free radicals are important for some essential biological
processes such as the killing of bacteria by neutrophils and certain cell signalling

Question 16

What factors influence mitochondria to produce ROS ?

Answer 16

Oxidative damage will impair mitochondrial function
Rate of O2 *- production is affected by mitochondrial metabolic state
Increased when electron carriers harbour excess electrons either from
inhibition of oxidative phosphorylation or excessive calorie consumption
Dysfunctional mitochondria produce more ROS and a feed-forward
loop is set up. Therefore ROS-mediated oxidative damage to mitochondria favours more ROS generation, resulting in a vicious cycle

Question 17

Explain the roles of enzymatic and non-enzymatic antioxidant defence mechanisms

Answer 17

Enzymatic Antioxidant Defense Mechanisms;
Superoxide Dismutase (SOD): Converts superoxide radicals into hydrogen peroxide which is degraded by glutathione
peroxidase (GPX) and peroxiredoxin
III (PrxIII)

Non-Enzymatic Antioxidant Defence Mechanisms;
Lipid peroxidation is prevented by
action of vitamin E and coenzyme Q
within phospholipid bilayer

Both prevent oxidative stress

Question 18

Describe the nature and impact of mitochondrial DNA (mtDNA) mutations induced by ROS and how they are inherited

Answer 18

mtDNA is near sites of ROS generation
Maternal inheritance for mtDNA
High levels of ROS produced during normal mitochondrial respiration and under pathological conditions increase the risk of mtDNA mutations
Mutations impair mitochondrial function by disrupting protein production in the ETC leading to decreased ATP production.