Energy metabolism of cultured TM4 cells and the action of gossypol.
Energy metabolism of cultured TM4 cells and the action of gossypol.
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DOI：
10.1095/biolreprod34.5.809
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发表时间：
1986-06
影响因子：
3.6
通讯作者：
Juan Reyes;L. Borriero;N. Tanphaichitr;A. Bellvé;D. J. Benos
中科院分区：
文献类型：
--
作者：
Juan Reyes;L. Borriero;N. Tanphaichitr;A. Bellvé;D. J. Benos
研究了原来源于小鼠睾丸细胞的TM4细胞的能量代谢与棉酚作用的关系。在没有外部添加底物的情况下，TM4细胞以37 +/- 5 nmol O2 X mg protein-1 X h-1的速度消耗氧气。丙酮酸以剂量依赖性的方式刺激氧气消耗高达23%。向悬浮在无底物培养基中的细胞中添加葡萄糖可抑制氧气消耗。在5.5 mM葡萄糖下，氧消耗抑制率为45 +/- 9%。内源性底物产生有氧乳酸的速率小于7 nmol乳酸X mg蛋白-1 X h-1，即使存在最佳浓度的线粒体解偶联剂羰基氰化间氯苯腙。在外部葡萄糖浓度为2mm或更高时，需氧乳酸生成速率为920 +/- 197 nmol X mg protein-1 X h-1。5 mM葡萄糖中需氧糖酵解三磷酸腺苷（ATP）的生成约占ATP总量的80%。棉酚以剂量依赖的方式刺激转化睾丸细胞的需氧乳酸产生和耗氧量。棉酚对葡萄糖运输、有氧乳酸生成和氧气消耗的影响与棉酚主要通过部分解偶联线粒体氧化磷酸化来改变这些细胞的能量代谢的假设一致。棉酚处理对细胞和组织功能可能造成的损害取决于每个特定分化细胞的代谢特性。
The energy metabolism of cultured TM4 cells, a cell line originally derived from mouse testicular cells, has been studied in relation to the action of gossypol. In the absence of externally added substrates, TM4 cells consumed oxygen at 37 +/- 5 nmoles O2 X mg protein-1 X h-1. Pyruvate stimulated oxygen consumption in a dose-dependent fashion up to 23%. Addition of glucose to the cells suspended in substrate-free medium inhibited oxygen consumption. At 5.5 mM glucose, the inhibition of oxygen consumption was 45 +/- 9%. The rate of aerobic lactate production from endogenous substrates was less than 7 nmoles lactate X mg protein-1 X h-1, even in the presence of optimal concentrations of the mitochondrial uncoupler carbonylcyanide m-chlorophenylhydrazone. The rate of aerobic lactate production was 920 +/- 197 nmoles X mg protein-1 X h-1 at external glucose concentrations of 2 mM or greater. The formation of aerobic glycolytic adenosine triphosphate (ATP) in 5 mM glucose comprised about 80% of the total ATP production. Gossypol stimulated both aerobic lactate production and oxygen consumption of the transformed testicular cells in a dose-dependent manner. The effect of gossypol on glucose transport, aerobic lactate production, and oxygen consumption is consistent with the hypothesis that gossypol modifies energy metabolism in these cells mainly by partially uncoupling mitochondrial oxidative phosphorylation. The possible impairment of cell and tissue function under gossypol treatment would depend on the metabolic properties of each specific differentiated cell.