Tapper H, Sundler R
Department of Medical and Physiological Chemistry, Lund University, Sweden.
Biochem J. 1992 Jan 1;281 ( Pt 1)(Pt 1):245-50. doi: 10.1042/bj2810245.
Recent evidence indicates that H+ extrusion in macrophages is in part accomplished by a H(+)-ATPase of vacuolar type. The presence and plasma-membrane localization of such a mechanism in adherent resident macrophages was verified by inhibition of H+ extrusion, monitored by changes in both cytosolic pH (pHi) and extracellular pH, with low concentrations of the H(+)-ATPase inhibitors N-ethylmaleimide and 7-chloro-4-nitrobenz-2-oxa-1,3-diazole. The H(+)-ATPase was operative at physiological pHi levels, thus contributing to maintenance of steady-state pHi. It was further shown to be sensitive to the plasma-membrane potential, with hyperpolarization being strongly inhibitory. In addition, H+ extrusion mediated by the H(+)-ATPase and the generation and release of lactic acid caused acidification of the pericellular space and could enable secreted lysosomal hydrolases to act extracellularly.
最近的证据表明，巨噬细胞中的H⁺排出部分是由液泡型H⁺-ATP酶完成的。通过用低浓度的H⁺-ATP酶抑制剂N-乙基马来酰亚胺和7-氯-4-硝基苯并-2-恶唑-1,3-二唑抑制H⁺排出（通过胞质pH（pHi）和细胞外pH的变化进行监测），证实了这种机制在贴壁驻留巨噬细胞中的存在及其质膜定位。H⁺-ATP酶在生理pHi水平下起作用，从而有助于维持稳态pHi。进一步表明它对质膜电位敏感，超极化具有强烈的抑制作用。此外，由H⁺-ATP酶介导的H⁺排出以及乳酸的产生和释放导致细胞周隙酸化，并可使分泌的溶酶体水解酶在细胞外发挥作用。
