ETC-UG notes.ppt

BC368
Electron Transport Chain
CH 19 (pp 731-747)
March 19, 2015
Biochemistry of the Cell II
http://www.science-groove.org/Now/Oxidative.html

Last fall, Michael Phelps was
pulled over in Baltimore after
police spotted him driving
erratically.
A Breathalyzer test revealed that Phelps’ blood alcohol content
was 0.14, well over the 0.08 legal limit.
Case Study

Ethanol is oxidized; dichromate
is reduced.
Reaction can be monitored
through a color change of the
chromium species.
Redox Reactions
2 Cr2O7
2- + 3 C2H5OH + 16 H+ --> 4 Cr3+ + 3 CH3CO + 11 H2O

Cr2O7
2- + 14 H+ + 6 e- --> 2 Cr3+ + 7 H2O
C2H5OH + H2O --> CH3COOH + 4 e- + 4 H+
Half Reactions
2 Cr2O7
2- + 3 C2H5OH + 16 H+ -->
4 Cr3+ + 3 CH3COOH + 11 H2O
Reduction (cathode)
Oxidation (anode)
Overall:

Half Reactions
In general,
’cell = ’cathode - ’anode
Higher tendency
for reduction
Lower tendency
for reduction
Reduced Oxidized
Standard reduction potentials are for reduction.

Cr2O7
2- + 14 H+ + 6 e- --> 2 Cr3+ + 7 H2O
C2H5OH --> CH3COOH + 2 e- + 2 H+
cell = 1.33 V - 0.058 V = 1.27 V
Half Reactions
Reduction (cathode);
 = 1.33 V
Oxidation (anode);
 = 0.058 V (for the reduction)

Half Reactions
In general,
’cell = ’cathode - ’anode
Reduced Oxidized
’cell > 0 is favorable
DG’ = -nF’cell

ATP is made through oxidative phosphorylation, powered
by the free energy released from electron transfer from
NADH to O2.
a) Given the following reduction potentials, calculate the
available standard free energy from this process.
NAD+ + H+ + 2 e-  NADH E’º = -0.32 V
1/2 O2 + 2 H+ + 2 e-  H2O E’º = 0.82 V
b) If three ATP ’ s are synthesized per electron pair
transferred, what is the efficiency of the process?
In-Class Problem

Chemiosmotic
Mechanism
Electron
transport chain
sets up an H+
gradient (proton
motive force).
Energy of the
pmf is harnessed
to make ATP.

Mitochondrion
Fig 19-2
 Double membrane, with
inner membrane very
impermeable
 TCA occurs in the matrix
 ETC in the inner
membrane

The patient was delivered by emergency C-section at 31
weeks of gestation. He required intubation in the delivery room
because of apnea and bradycardia and was treated in the
Neonatal Intensive Care Unit. A follow-up chest X-ray taken at
1 month of age showed an enlarged heart and prompted a
cardiology consult. Although there was no clinical evidence
of congestive heart failure, the cardiac ultrasound showed a
significant decrease in left ventricular function. The family
history was significant in that the patient’s maternal uncle died
from sudden infant death syndrome.
At 11 months of age, the patient’s mother was concerned
about his poor weight gain and development because he was
not yet sitting alone.
Case Study

At his 20th-month visit, persistent muscle weakness, growth
delays, and congestive cardiomyopathy led the cardiologist to
make a genetics referral. Two days following this clinic visit,
however, the patient presented to his primary care provider with
cough, wheezing, runny nose, and one day of fever and mental
status change.
His condition deteriorated, requiring intubation, and he was
transferred to the Pediatric Intensive Care Unit. The diagnosis
was pneumonia, and severe lactic acidosis was found. He failed
to respond to aggressive treatment and died from repeated
ventricular fibrillation that occurred 10 days later.
Autopsy limited to the heart was performed. The gross and
microscopic findings were characteristic of Barth syndrome.
The heart weighed 100 g (average for his age is 56 g, and 100 g
is the average for a 7-year-old).
Case Study

A small number of boys suffer
from Barth syndrome (~50
births/year in the United States).
Patients with Barth syndrome have abnormal
mitochondria and cannot maintain normal rates of
ATP production. These patients develop life-
threatening cardiomyopathy and muscle weakness.
Barth’s results from a mutation
on the X chromosome in the
gene coding for taffazin, an
enzyme involved in the
biosynthesis of cardiolipin.
Cardiolipin

ETC carriers: Coenzyme Q
Fig 19-3
 Mobile
electron
carrier within
the bilayer
 1- or 2-
electron
acceptor

ETC carriers: FMN
 Prosthetic group
of ETC protein
(complex I)
 1- or 2-electron
acceptor

ETC carriers: Cytochromes
 Heme proteins
 Cytochrome c is a
soluble peripheral
protein
 Most are integral
proteins

ETC carriers: Iron-sulfur proteins
Fig 19-5

ETC carriers: Copper centers
 CuA center  CuB center

Electron Transport Chain: Proteins

~Fig 19-16

Alternate Entries
Complex II
(aka succinate
dehydrogenase)

 Electrons flow from carriers
with low to high reduction
potential.
Succinate
dehydrogenase
 This is energetically downhill.

 Some carriers pump protons.
Succinate
dehydrogenase
4 H+
in
4 H+
in
2 H+
in
Per electron
pair:
2 H+
out
4 H+
out
4 H+
out

Inhibitors of electron transport
Fig 19-6

Case Study
Four carriers (a, b, c, d) are required for respiration in a novel
bacterial electron-transport system. In the presence of
substrate and O2, three different inhibitors block respiration as
shown. What is the order of carriers?
Inhibitor a b c d
1 + + - +
2 - - - +
3 + - - +
“+” = fully oxidized; “-” = fully reduced

O2 consumption as a measure
of electron transport
 An oxygen electrode can measure O2 consumption in
respiring mitochondria.

O2 consumption as a measure
of electron transport
 An oxygen electrode can measure O2 consumption in
respiring mitochondria.
Substrate added
Substrate
consumed

Coupling of electron transport
and ATP synthesis
 Data can be
reported as O2
concentration
or O2
consumption.

Coupling of electron transport
and ATP synthesis
Fig 19-20

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