Appaix 2002 Biochim Biophys Acta
|Appaix F, Guerrero K, Rampal D, Izikki M, Kaambre T, Sikk P, Brdiczka D, Riva-Lavieille C, Olivares J, Longuet M, Antonsson B, Saks VA (2002) Bax and heart mitochondria: uncoupling and inhibition of respiration without permeability transition. Biochim Biophys Acta 1556:155-67.|
Abstract: The effects of Bax (full-length, FL, and C-terminal truncated, ΔC) on respiration rate, membrane potential, MgATPase activity and kinetics of regulation of respiration were studied in isolated rat heart mitochondria and permeabilized cardiomyocytes. The results showed that while both Bax-FL and Bax-ΔC permeabilized the outer mitochondrial membrane, released cytochrome c and reduced the respiration rate, the latter could be fully restored by exogenous cytochrome c only in the case of Bax-ΔC, but not in presence of Bax-FL. In addition, Bax-FL but not Bax-ΔC increased the MgATPase activity, and their effects on the mitochondrial membrane potential were quantitatively different. None of these effects was sensitive to cyclosporin A (CsA).
It is concluded that Bax-FL affects both the outer and the inner mitochondrial membranes by: (1) opening large pores in the outer membrane; (2) inhibiting some segments of the respiratory chain in the inner membrane; and (3) uncoupling the inner mitochondrial membrane by increasing proton leak without opening the permeability transition pore (PTP). • Keywords: Mitochondrion, Apoptosis, Heart, Oxidative phosphorylation, Bax
Labels: MiParea: Respiration
Organism: Rat Tissue;cell: Heart Preparation: Permeabilized cells, Isolated mitochondria
Regulation: ADP, ATP