Triphenyltin as inductor of mitochondrial membrane permeability transition.
The effect of triphenyltin on mitochondrial Ca2+ content was studied. It was found that this trialkyltin compound induces an increase in membrane permeability that leads to Ca2+ release, drop of the transmembrane potential, and efflux of matrix proteins. Interestingly, cyclosporin A was unable to inhibit triphenyltin-induced Ca2+ release. Based on these results it is proposed that the hyperpermeable state is produced by modification of 2.25 nmol of membrane thiol groups.
Departamento de Bioquímica, Instituto Nacional de Cardiologia, Ignacio Chavez, México, D. F., México.
C
C
Zazueta
H
H
Reyes-Vivas
C
C
Bravo
J
J
Pichardo
N
N
Corona
E
E
Chávez
D000818:Animals; D002118:Calcium / Q000378:metabolism; D016572:Cyclosporine / Q000494:pharmacology; D003545:Cysteine / Q000378:metabolism; D004229:Dithiothreitol / Q000494:pharmacology; D007425:Intracellular Membranes / Q000187:drug effects* / Q000378:metabolism; D007668:Kidney; D008565:Membrane Proteins / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D009947:Organotin Compounds / Q000494:pharmacology*; D010539:Permeability / Q000187:drug effects; D051381:Rats
D008565:Membrane Proteins; D009947:Organotin Compounds; D016572:Cyclosporine; C030665:triphenyltin; D003545:Cysteine; D002118:Calcium; D004229:Dithiothreitol