Ito E, Sakihama H, Toyama K, Matsui K
Cancer Res. 1984 May;44(5):1985-90.
The heat produced by Ehrlich ascites carcinoma cells was measured microcalorimetrically to investigate the characteristics of the energetics of these cells. 2,4-Dinitrophenol and other inhibitors were used to obtain the standard thermograms. The heat level of starved Ehrlich ascites carcinoma cells (endogenous) was almost constant and linear and depended on the cell number used in the experiments (about 1 cal/1 X 10(8) cells/hr). The endogenous heat generation was suppressed strongly by potassium cyanide but not by iodoacetic acid or 2,4-dinitrophenol. On the other hand, heat evolution was directly related to the amount of glucose added to the medium but not to the number of cells (19 cal/mmol of glucose). The addition of iodoacetic acid markedly suppressed heat generation, but potassium cyanide did not. In contrast, glucose with dinitrophenol increased heat production markedly to about 10% higher than that of the control, possibly due to the uncoupled energy from oxidative phosphorylation. Malonic acid (1 mM) suppressed slightly the endogenous heat but caused a 15% reduction in exogenous heat. The amount of heat produced by the addition of glucose (19 cal/mmol) was equivalent to 40% of the theoretical value of energy released through glycolysis (47 cal/mmol). Thus, the heat produced by exogenous glucose appears to be mainly dependent on glycolysis.
采用微量量热法测定艾氏腹水癌细胞产生的热量，以研究这些细胞的能量学特征。使用2,4-二硝基苯酚和其他抑制剂来获得标准热谱图。饥饿的艾氏腹水癌细胞（内源性）的热量水平几乎恒定且呈线性，并且取决于实验中使用的细胞数量（约1卡/1×10⁸个细胞/小时）。内源性产热受到氰化钾的强烈抑制，但不受碘乙酸或2,4-二硝基苯酚的抑制。另一方面，热量释放与添加到培养基中的葡萄糖量直接相关，而与细胞数量无关（19卡/毫摩尔葡萄糖）。添加碘乙酸显著抑制产热，但氰化钾则没有。相比之下，葡萄糖与二硝基苯酚一起显著增加产热，比对照高出约10%，这可能是由于氧化磷酸化的能量解偶联所致。丙二酸（1毫摩尔）略微抑制内源性热量，但使外源性热量减少15%。添加葡萄糖（19卡/毫摩尔）产生的热量相当于通过糖酵解释放的能量理论值的40%（47卡/毫摩尔）。因此，外源性葡萄糖产生的热量似乎主要依赖于糖酵解。
