Lactate release and uptake in hepatoma 7288CTC perfused in situ with L-[(U)-14C]lactate or D-[(U)-14C]glucose.
Lactate release and uptake in hepatoma 7288CTC perfused in situ with L-[(U)-14C]lactate or D-[(U)-14C]glucose.
复制标题
用 L-[(U)-14C]乳酸或 D-[(U)-14C]葡萄糖原位灌注的肝癌 7288CTC 中乳酸的释放和摄取。
DOI：
10.1016/0026-0495(94)90006-x
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Dauchy,RT
中科院分区：
文献类型：
--
作者：
Sauer,LA;Dauchy,RT
Arteriovenous differences (AVD) for glucose and lactic acid measured across tissue-isolated rat tumors in vivo have shown that individual tumors with similar rates of glucose consumption may either release or utilize lactic acid. The experiments described here investigated the relationships among arterial blood lactate concentrations and tumor lactate and glucose balances. AVDs for lactate, pyruvate, glucose,14CO2, Po2, Pco2, pH, and lactate specific activities were measured across 17 tissue-isolated 7288CTC hepatomas perfused in situ with arterial blood containing 2.5 to 14.4 mmol/L lactate and eitherl-[(U)-14C]lactic acid ord-[(U)-14C]glucose. Measurements were made over a range of blood flow rates from 60% to 200% of the mean in vivo rate, 0.11 mL/min. Data collected during steady states were compared by regression analysis. Tumor lactate balance and the arterial blood lactate concentration were directly related (r= .895, n = 22,P< .01). Net negative and positive balances occurred below and above approximately 6.5 mmol/L arterial blood lactate, respectively. The mean intratumor lactate concentration for all tumors was 6.9 ± 1.0 mmol/L (mean ± SD, n = 13). Rates of14C-lactate oxidation to14CO2(r= .716, n = 18,P< .01) and tumor venous / arterial blood14C-lactate specific activity ratios (r= .845, n = 19,P< .01) were low during lactate release and were increased during lactate uptake. Total arterial blood lactate removal estimated from chemical and isotopic analyses was 23.1% ± 11% and 43.0% ± 16% (P< .05), respectively, for six lactate-utilizing tumors. Perfusions performed with14C-glucose showed that approximately 50% of the glucose consumed during net negative lactate balance was released as14C-lactate to the tumor venous blood, whereas only 5% was released as14C-lactate during net positive lactate balance. The data support the following conclusions: Arterial blood lactate controls net lactate balance in solid tumors; high concentrations increase uptake. Lactate uptake inhibits lactate formation from glucose without changing the glucose balance. Lactate is released during net lactate uptake. Since lactate uptake may exceed glucose uptake, arterial blood lactate can be a substrate for tumor energy metabolism and growth.
