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.
Zazueta
C
C
Departamento de Bioquímica, Instituto Nacional de Cardiologia, Ignacio Chavez, México, D. F., México.
Reyes-Vivas
H
H
Bravo
C
C
Pichardo
J
J
Corona
N
N
Chávez
E
E
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