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How does antimycin inhibit the bc1 complex? A part-time twin.

Stéphane Ransac¹, Jean-Pierre Mazat

¹Université de Bordeaux 2, 146 rue Léo-Saignat, F 33076, Bordeaux cedex, France.

Biochimica Et Biophysica Acta

|June 10, 2010

Summary

Antimycin inhibition of the bc(1) complex requires blocking electron return to the Q(o) site. This leads to a unique dimer interface electron transfer pathway, explaining observed inhibition and ROS production.

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Area of Science:

Biochemistry
Bioenergetics
Enzyme kinetics

Background:

The bc(1) complex is crucial for cellular respiration and ATP production.
Previous models explained the Q-cycle but not antimycin inhibition or ROS production.

Purpose of the Study:

To elucidate the mechanism of antimycin inhibition in the bc(1) complex.
To explain the associated increase in reactive oxygen species (ROS) production.

Main Methods:

Stochastic simulations of the bc(1) complex.
Incorporation of hypotheses regarding electron transfer pathways and antimycin binding.

Main Results:

A modified Mitchell Q-cycle emerges naturally in simulations.
Blocking electron return from reduced heme b(L) to Q(o) is necessary for inhibition.
A sigmoid inhibition curve arises from inter-monomer electron transfer at the dimer interface when antimycin is half-bound.
Half-of-the-sites reactivity explains transient activation before complete inhibition.

Conclusions:

Antimycin inhibition involves a specific electron transfer pathway across the bc(1) dimer interface.
The model successfully explains both inhibition kinetics and ROS production.
Understanding these mechanisms is vital for bioenergetics and drug development targeting the bc(1) complex.