BC368 Electron Transport Chain CH 19 (pp 731-747) March 19, 2015 Biochemistry of the Cell II

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 Cr2O72-

+ 3 C2H5OH + 16 H+ --> 4 Cr3+ + 3 CH3CO + 11 H2O

Cr2O72-

+ 14 H+ + 6 e- --> 2 Cr3+ + 7 H2O

C2H5OH + H2O --> CH3COOH + 4 e- + 4 H+

Half Reactions

2 Cr2O72-

+ 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.

Cr2O72-

+ 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

G’ = -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 V1/2 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

ETC Video

Chemiosmotic Mechanism

Electron transport chain sets up an H+ gradient (proton motive force).

Energy of the pmf is harnessed to make ATP.

MitochondrionFig 19-2

Double membrane, with inner membrane very impermeable

TCA occurs in the matrix

ETC in the inner membrane

Cardiolipin

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 evidenceof 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

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

Electron transport chain

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

Complex I

Alternate Entries

Fig 19-8

Alternate Entries

Complex II (aka succinate dehydrogenase)

Alternate Entries

Fig 19-8

Alternate Entries

Fig 19-8


Complex III

Complex III

Fig 19-11


Complex IV

Fig 19-14

Complex IV

Electrons flow from carriers with low to high reduction potential.

Succinate dehydrogenase


This is energetically downhill.

Some carriers pump protons.

Succinate dehydrogenase

Electron Transport Chain4 H+ in

4 H+ in

2 H+ in

Per electron pair:

2 H+ out

4 H+ out

4 H+ out

Flow direction

Flow direction

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

Q Cycle

Q Cycle

Q Cycle

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.


Fig 19-20


Fig 19-20

Documents

BC368 Electron Transport Chain CH 19 (pp 731-747) March 19, 2015 Biochemistry of the Cell II