Intracellular shunting of O2(-) contributes to charge compensation and preservation of neutrophil respiratory burst in the absence of voltage-gated proton channel activity.

ABSTRACT: Proton efflux via voltage-gated proton channels (Hv1) is considered to mediate the charge compensation necessary to preserve NADPH oxidase activity during the respiratory burst. Using the Hv1 inhibitor Zn(2+), we found that the PMA-induced respiratory burst of human neutrophils is inhibited when assessed as extracellular production of O2(-) and H2O2, in accordance with literature studies, but, surprisingly, unaffected when measured as oxygen consumption or total (extracellular plus intracellular) H2O2 production. Furthermore, we show that inhibiting Hv1 with Zn(2+) results in an increased production of intracellular ROS. Similar results, i.e. decreased extracellular and increased intracellular ROS production, were obtained using a human granulocyte-like cell line with severely impaired Hv1

SUBMITTER: Decleva E 

PROVIDER: S-EPMC3712189 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature