Riquelme G, Jaimovich E, Lingsch C, Behn C
Biochim Biophys Acta. 1982 Jul 28;689(2):219-29. doi: 10.1016/0005-2736(82)90254-1.
Chemically induced shape changes of the human erythrocyte may result from cell membrane bending by surface tension changes at the lipid bilayer (Evans. E.A. (1974( Biophys. J. 14, 923-931) implicating differential expansion of the monolayers coupled to form the red cell membrane (Sheetz, M.P. and Singer, S.J. (1974) Proc. Natl. Acad. Sci. U.S.A. 71, 4457-4461). Interacting with calcium, the antibiotic chlorotetracycline (CTC) transforms crenated cells (echinocytes) into cup-shaped ones (stomatocytes), presumably expanding thereby the red cell membrane inner leaflet relative to the outer one (Behn, C., Lübbemeier, A. and Weskamp, P. (1977) Pflügers Arch. 372, 259-268). Whether the Ca-CTC interaction with lipid monolayers may in fact expand the latter, has now been examined by surface tension measurements at the air/water interface. CTC and lipids appeared to compete for the available sites at the air/water interface, contributing additively to its surface pressure. Ca increased both the adsorption rate of the antibiotic to the interface and the CTC-induced surface pressure increment. The latter was not influenced by the subphase pH and ionic strength, or by the type of phospholipid polar head. Correspondingly, CTC-induced cell shape changes should be determined by the pCa values facing either monolayer of the erythrocyte membrane. Both stomatocytes and echinocytes could indeed by obtained with 0.5 mmol . 1(-1) CTC, the cell shape depending on whether the external medium was adjusted respectively to pCa 9 or to pCa 3. Fluorescence microscopy revealed the Ca-CTC complex to be mostly restricted to the cell in stomatocytes and to the external medium in echinocytes. The possibility of inducing alternative cell shapes by varying the transmembrane Ca-CTC distribution, and the demonstration of a Ca-dependent expansion of even relatively compressed lipid monolayers by CTC, together suggest that the Ca-CTC complex may also differentially expand either leaflet of the red cell membrane.
化学诱导的人类红细胞形状变化可能源于脂质双层表面张力变化导致的细胞膜弯曲（埃文斯，E.A.（1974年）《生物物理杂志》14卷，923 - 931页），这暗示了形成红细胞膜的单分子层的差异膨胀（希茨，M.P.和辛格，S.J.（1974年）《美国国家科学院院刊》71卷，4457 - 4461页）。抗生素氯四环素（CTC）与钙相互作用，将皱缩细胞（棘状红细胞）转变为杯状细胞（口形红细胞），推测由此使红细胞膜内小叶相对于外小叶扩张（贝恩，C.、吕贝迈尔，A.和韦斯卡姆普，P.（1977年）《 Pflügers 文献》372卷，259 - 268页）。Ca - CTC与脂质单分子层的相互作用是否实际上会使后者扩张，现已通过在空气/水界面进行表面张力测量来研究。CTC和脂质似乎在空气/水界面竞争可用位点，对其表面压力有累加贡献。Ca增加了抗生素在界面的吸附速率以及CTC诱导的表面压力增量。后者不受亚相pH值和离子强度或磷脂极性头部类型的影响。相应地，CTC诱导的细胞形状变化应由面向红细胞膜任一单分子层的pCa值决定。用0.5 mmol·1⁻¹ CTC确实可以得到口形红细胞和棘状红细胞，细胞形状取决于外部介质分别调整到pCa 9还是pCa 3。荧光显微镜显示Ca - CTC复合物在口形红细胞中大多局限于细胞内，而在棘状红细胞中则存在于外部介质中。通过改变跨膜Ca - CTC分布诱导替代细胞形状的可能性，以及CTC对即使相对压缩的脂质单分子层的钙依赖性扩张的证明，共同表明Ca - CTC复合物也可能使红细胞膜的任一小叶有差异地扩张。
