Floridi A, Barbieri R, Pulselli R, Fanciulli M, Arcuri E
Laboratory of Cell Metabolism and Pharmacokinetics, Regina Elena Institute for Cancer Research, Rome, Italy.
Oncol Res. 1994;6(12):593-601.
The effect of the local anesthetic bupivacaine on the energy metabolism of Ehrlich ascites tumor cells has been investigated. Even at low concentrations, bupivacaine decreased the oxygen uptake rate, but its effect was remarkably higher on the uncoupled respiration. Experiments on specific segments of the respiratory chain have shown that bupivacaine did not inhibit electron transport from Q to oxygen. Spectroscopic evidences demonstrated a NAD(P)H oxidation in bupivacaine-treated cells respiring on endogenous substrates, indicating that the inhibition of oxygen depended on a reduced electron transport from site 1-entering substrates to respiratory chain. The aerobic glycolysis was stimulated by low and inhibited by high bupivacaine concentrations. The increased lactate production rate was due to an activation of mitochondrial ATPase, whereas its decrease was related to an inhibition of the hexokinase activity.
研究了局部麻醉药布比卡因对艾氏腹水癌细胞能量代谢的影响。即使在低浓度下，布比卡因也会降低氧摄取率，但其对解偶联呼吸的影响显著更高。对呼吸链特定部分的实验表明，布比卡因并不抑制从辅酶Q到氧的电子传递。光谱证据表明，在以内源性底物呼吸的布比卡因处理细胞中存在烟酰胺腺嘌呤二核苷酸（磷酸）（NAD(P)H）氧化，这表明氧的抑制取决于从进入底物的位点1到呼吸链的电子传递减少。低浓度布比卡因刺激有氧糖酵解，高浓度则抑制。乳酸产生率的增加是由于线粒体ATP酶的激活，而其降低与己糖激酶活性的抑制有关。
