Regen D M, Tarpley H L
Biochim Biophys Acta. 1978 Apr 20;508(3):539-50. doi: 10.1016/0005-2736(78)90098-6.
Entry of beta-hydroxybutyrate into erythrocytes and thymocytes is facilitated by a carrier (C), as judged from temperature dependence, saturation kinetics, stereospecificity, competition with lactate and pyruvate, and inhibition by moderate concentrations of methylisobutylxanthine, phloretin, or alpha-cyanocinnamate. We studied the dependence of influx and efflux on internal and external pH and [beta-hydroxybutyrate]. Lowering external pH from 8.0 to 7.3 to 6.6 enhanced influx into erythrocytes by lowering entry Km from 29 to 16 to 10 mM, entry V being independent of external pH. Lowering external pH inhibited efflux. At low external pH, external beta-hydroxybutyrate enhanced efflux slightly. At high external pH, external beta-hydroxybutyrate inhibited efflux. Internal acidification inhibited influx and internal alkalization enhanced influx. Internal beta-hydroxybutyrate (betaHB) enhanced influx more in acidified than alkalized cells. These data are compatible with coupled betaHB-/OH- exchange, betaHB- and OH- competing for influx, C:OH- moving faster than C: betaHB-, empty C being immobile. They are also compatible with coupled betaHB-/H+ copermeation, empty C moving inward faster than H+:C:betaHB-, H+:C being immobile, and C:betaHB- (without H+) being so unstable as not to be formed in significant amounts (relative to C, H+:C, and H+:C:betaHB-).
从温度依赖性、饱和动力学、立体特异性、与乳酸和丙酮酸的竞争性以及中等浓度的甲基异丁基黄嘌呤、根皮素或α-氰基肉桂酸酯的抑制作用判断，β-羟基丁酸通过载体（C）进入红细胞和胸腺细胞。我们研究了流入和流出对细胞内、外pH值和[β-羟基丁酸]的依赖性。将外部pH值从8.0降至7.3再降至6.6，通过将进入的Km从29 mM降至16 mM再降至10 mM，增强了β-羟基丁酸进入红细胞的能力，进入的V与外部pH值无关。降低外部pH值抑制流出。在低外部pH值下，外部β-羟基丁酸略微增强流出。在高外部pH值下，外部β-羟基丁酸抑制流出。细胞内酸化抑制流入，细胞内碱化增强流入。细胞内β-羟基丁酸（βHB）在酸化细胞中比在碱化细胞中更能增强流入。这些数据与βHB-/OH-耦合交换、βHB-和OH-竞争流入、C:OH-比C:βHB-移动得更快、空的C不移动相一致。它们也与βHB-/H+耦合共渗透、空的C向内移动比H+:C:βHB-更快、H+:C不移动以及C:βHB-（无H+）非常不稳定以至于不会大量形成（相对于C、H+:C和H+:C:βHB-）相一致。
