EXOGENOUS LACTATE INTERFERES WITH CELL-CYCLE CONTROL IN BALB/3T3 MOUSE FIBROBLASTS
EXOGENOUS LACTATE INTERFERES WITH CELL-CYCLE CONTROL IN BALB/3T3 MOUSE FIBROBLASTS
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DOI：
10.1016/0360-3016(94)00362-o
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发表时间：
1995-02-01
影响因子：
7
通讯作者：
LITTLE, JB
中科院分区：
文献类型：
--
作者：
RUTZ, HP;LITTLE, JB
目的：已有研究表明，外源性乳酸可影响哺乳动物细胞的增殖速率、辐射敏感性和辐射后修复能力。在本研究中，我们解决了潜在的潜在机制的问题，因此，研究外源性乳酸对增殖率和细胞周期分布在不朽的，但nontumorigenic mammalian cells. Methods和Materials的影响：细胞仅仅生长在37摄氏度的培养箱中，5%CO2和95%的空气，在培养基中补充或不与乳酸在10 mM的浓度。每天，我们更换培养基并计数每个培养皿的细胞。在选定的天数，通过流式细胞术测定细胞周期分布。结果：在细胞增殖的指数期，由于选择性地延长了G2/M期，平均群体倍增时间从17.7 h显著增加到19.9 h。然而，在密度抑制的文化，外源性乳酸刺激进入S和增殖到一个显着较高的饱和density.Conclusions：这些研究结果表明，外源性乳酸干扰机制的细胞周期控制在两个不同的点在细胞周期中，取决于细胞密度和由此产生的不存在或存在的抑制细胞增殖。细胞周期调控的干扰可能是外源性乳酸修饰哺乳动物细胞辐射敏感性和辐射后修复能力的基础。
Purpose: Previous studies have shown that exogenous lactate may influence proliferation rates, radiation sensitivity, and postirradiation repair capacity of mammalian cells. In the present study, we addressed the question of potential underlying mechanisms and, therefore, examined effects of exogenous lactate on proliferation rates and cell-cycle distribution in immortal but nontumorigenic mammalian cells.Methods and Materials: Cells mere grown at 37 degrees C in an incubator with 5% CO2 and 95% air, in a culture medium supplemented or not with lactate at a 10 mM concentration. Daily, we changed the culture medium and counted cells per dish. On selected days, cell-cycle distribution was determined by flow cytometry. Balb/3T3 mouse fibroblasts were used.Results: During the exponential phase of cell proliferation, mean population doubling time was significantly increased from 17.7 to 19.9 h, due to selective prolongation of G(2)/M. However, in density-inhibited cultures, exogenous lactate stimulated entry into S and proliferation to a significantly higher saturation density .Conclusions: These findings indicate that exogenous lactate interferes with mechanisms of cell-cycle control at two different points in the cell-cycle, depending on cell density and the resulting absence or presence of inhibition of cell proliferation. Interference with cell-cycle control may underly the modification by exogenous lactate of radiosensitivity and postirradiation repair capacity in mammalian cells.