Cramer W A, Postma P W, Helgerson S L
Biochim Biophys Acta. 1976 Dec 6;449(3):401-11. doi: 10.1016/0005-2728(76)90151-1.
Colicin El and the uncoupler of oxidative phosphorylation, trifluoromethoxy-carbonylcyanidephenylhydrazone (FCCP), cause an increase in the fluorescence intensity of N-phenyl-1-naphthylamine bound to whole cells of Escherichia coli. It has been shown elsewhere that this fluorescence increase correlates well with de-energization. Addition of glucose causes a large cyanide-sensitive decrease of intensity, tentatively associated with energization, with the emission spectrum almost returning to the original trace with a peak at 417 nm. These data suggest that there may be a measurable competition between de-energization and energization of the cell membrane, and that the probe fluorescence intensity may be a general indicator of membrane energy level. The conclusions reached about cellular energy level from measurements of the probe fluorescence intensity correlate partly (a, b below, not c) with the energy level assayed physiologically through rates of active transport; (a) FCCP is found to be a poor inhibitor of proline transport if cells are first incubated with glucose, showing eutger cinpetition between the processes of energization and de-energization or an increase in the envelope permeability barrier to FCCP caused by glucose addition. (b) Cyanide blocks the fluorescence decrease caused by glucose and inhibits proline and serine transport, consistent with the decrease in probe fluorescence intensity indicating an increase in membrane energization. However, (c) it appears that the amplitude of the fluorescence intensity decrease caused by glucose addition in the presence of FCCP and colicin E1 greatly exaggerates the extent of real membrane energization. Glucose added after uncoupler can cause only a small increase, and after colicin, a negligible increase in the proline transport rate, indicating that the magnitude of the fluorescence intensity decrease after glucose addition is not a true measure of membrane energization, but rather seems to amplify this energization greatly. Glucose addition does not cause a decrease in fluorescence intensity in cells treated with EDTA to remove lipopolysaccharide and an apparent barrier to the probe. The rotational relaxation time of the probe in intact cells appears to correlate somewhat better with the cellular energy level than does intensity.
大肠菌素E1和氧化磷酸化解偶联剂三氟甲氧基羰基氰基苯腙(FCCP)会使与大肠杆菌全细胞结合的N-苯基-1-萘胺的荧光强度增加。其他研究表明,这种荧光增强与去能化密切相关。添加葡萄糖会导致强度大幅下降,且对氰化物敏感,这初步与供能化相关,发射光谱几乎恢复到原始轨迹,峰值在417nm。这些数据表明,细胞膜的去能化和供能化之间可能存在可测量的竞争,且探针荧光强度可能是膜能量水平的通用指标。通过测量探针荧光强度得出的关于细胞能量水平的结论,部分(如下文a、b,而非c)与通过主动运输速率进行生理测定的能量水平相关;(a)如果细胞先与葡萄糖孵育,发现FCCP是脯氨酸运输的弱抑制剂,这表明供能化和去能化过程之间存在竞争,或者添加葡萄糖导致包膜对FCCP的通透性屏障增加。(b)氰化物会阻止葡萄糖引起的荧光下降,并抑制脯氨酸和丝氨酸运输,这与探针荧光强度的下降表明膜供能化增加一致。然而,(c)在FCCP和大肠菌素E1存在的情况下,添加葡萄糖引起的荧光强度下降幅度似乎极大地夸大了实际膜供能化的程度。在解偶联剂之后添加葡萄糖只会导致脯氨酸运输速率有小幅增加,而在大肠菌素之后添加葡萄糖,脯氨酸运输速率的增加可忽略不计,这表明添加葡萄糖后荧光强度下降的幅度并非膜供能化的真实度量,而似乎是极大地放大了这种供能化。在用EDTA处理以去除脂多糖和对探针的明显屏障的细胞中,添加葡萄糖不会导致荧光强度下降。完整细胞中探针的旋转弛豫时间似乎比强度与细胞能量水平的相关性稍好一些。