Abstract
In this paper we introduce monobromobimane, a thiol reagent, as a selective blocker of the recently identified dithiol whose oxidation-reduction status modifies voltage sensing by the mitochondrial permeability transition pore, a cyclosporin A-sensitive channel. Monobromobimane does not inhibit the phosphate carrier, nor does it interfere with Ca2+ transport, energy coupling or ATP production and transport. We show that monobromobimane selectively prevents the shift in pore gating potential caused by some dithiol oxidants or crosslinkers but not by increasing [Ca2+], allowing a clear distinction of the pore agonists which act at this site.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenosine Triphosphate / metabolism
-
Animals
-
Bridged Bicyclo Compounds / pharmacology*
-
Calcium / metabolism
-
Calcium Channels / metabolism
-
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology
-
Cyclosporine / pharmacology
-
Intracellular Membranes / drug effects
-
Ion Channel Gating / drug effects
-
Ion Channels / antagonists & inhibitors*
-
Mitochondria, Liver / drug effects*
-
Mitochondria, Liver / metabolism
-
Oxidation-Reduction
-
Oxygen Consumption / drug effects
-
Permeability / drug effects
-
Phosphates / metabolism
-
Rats
-
Toluene / analogs & derivatives*
-
Toluene / antagonists & inhibitors
Substances
-
Bridged Bicyclo Compounds
-
Calcium Channels
-
Ion Channels
-
Phosphates
-
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
-
Toluene
-
Cyclosporine
-
Adenosine Triphosphate
-
Calcium
-
dithiol
-
monobromobimane