Anion transport across phospholipid membranes mediated by a diphosphine–Pd(ii) complex

2014 ◽  
Vol 50 (65) ◽  
pp. 9157 ◽  
Author(s):  
Domenico Milano ◽  
Barnaba Benedetti ◽  
Mariangela Boccalon ◽  
Andrea Brugnara ◽  
Elisabetta Iengo ◽  
...  
Keyword(s):  
Anion Transport ◽  
Phospholipid Membranes

scholarly journals Redox-controlled chalcogen and pnictogen bonding: the case of a sulfonium/stibonium dication as a preanionophore for chloride anion transport

2020 ◽  
Vol 11 (37) ◽  
pp. 10107-10112
Author(s):  
Gyeongjin Park ◽  
François P. Gabbaï
Keyword(s):  
Anion Transport ◽  
Chloride Anion ◽  
Phospholipid Membranes

We describe a sulfonium/stibonium dication that behaves as a preanionophore activatable by glutathione (GSH). Indeed, this dication is reduced by GSH to yield a thioether/stibonium monocation that readily transports Cl− across phospholipid membranes.

Association of the polioviral RNA polymerase complex with phospholipid membranes.

1976 ◽  
Vol 19 (2) ◽  
pp. 457-466 ◽  
Author(s):  
B E Butterworth ◽  
E J Shimshick ◽  
F H Yin
Keyword(s):  
Rna Polymerase ◽  
Phospholipid Membranes ◽  
Polymerase Complex

A Class of Drugs that Inhibits Platelet Release and Aggregation by Apparent Interference with Anion Transport

1979 ◽  
Author(s):  
N.R. Shulman ◽  
H.B. Pollard ◽  
K. Tack-Goldman
Keyword(s):  
Pyridoxal Phosphate ◽  
Human Platelets ◽  
Anion Transport ◽  
Serotonin Release ◽  
Secretory Cells ◽  
Chloride Uptake ◽  
Potential Alternative ◽  
Osmotic Lysis ◽  
Platelet Release ◽  
Ph Range

The platelet release reaction is analogous to the process of exocytosis by which many other secretory cells release hormones or mediators from intracellular granules. Anion transport blocking (ATB) drugs Inhibit release of epinephrine from isolated chromaffin granules (CG) by blocking chloride uptake and preventing osmotic lysis. Studies on platelets analagous to those done on CG showed that increasing osmotic strength in the range 600-1000 m0sm progressively suppressed serotonin release to completion and that ATB drugs (viz, probenecid, SITS, pyridoxal phosphate and suramin) at mM concentrations completely inhibited release and aggregation of human platelets stimulated by thrombin, ADP, A23187, epinephrine or collagen. Sulfinpyrazone has the appropriate structure for anionic blocking, and may suppress platelet function as effectively by this mechanism as by cycloxy-genase inhibition. The ATB drugs acted apparently to prevent movement of OH- from the more alkaline medium into the relatively acidic granule, for platelet release was not inhibited by replacing anions with isethionate or sucrose, but was markedly dependent on OH- in the pH range 6 to 7.5 where inhibition by the ATB drugs was competitive with respect to OH-. Since the ATB compounds include some relatively nontoxic drugs in common use, and since their action on platelets differs markedly from that of aspirin, they should receive attention as potential alternative or auxiliary antithrombotic agents.

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