Abstract:
:We present evidence that the potent chloride channel blocker NPPB has protonophoric activity in the mitochondria and across the plasma membrane of phagocytic cells. The resting O2 consumption of murine peritoneal macrophages was stimulated up to 2.5-fold in the presence of NPPB, with a K0.5 of 15 microM. The stimulatory effect of NPPB on O2 consumption, like that of the classical protonophore CCCP, was prevented by the mitochondrial respiratory chain inhibitors antimycin A, rotenone or cyanide. NPPB also mediated rheogenic proton transport across the plasma membrane of human neutrophils and macrophages in the direction dictated by the electrochemical proton gradient. As a consequence of its protonophoric activity, NPPB uncoupled mitochondrial ATP synthesis, resulting in partial depletion of cellular ATP. These observations indicate that, at the concentrations frequently used for blockade of anion channels, NPPB acts as an effective protonophore, potentially disturbing cytosolic pH and mitochondrial ATP synthesis.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Lukacs GL,Nanda A,Rotstein OD,Grinstein Sdoi
10.1016/0014-5793(91)80992-ckeywords:
subject
Has Abstractpub_date
1991-08-19 00:00:00pages
17-20issue
1-2eissn
0014-5793issn
1873-3468pii
0014-5793(91)80992-Cjournal_volume
288pub_type
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