Portolés M T, Pagani R, Díaz-Laviada I, Municio A M
Cell Biochem Funct. 1987 Jan;5(1):55-61. doi: 10.1002/cbf.290050107.
The fluorescence probe 1,6-diphenylhexa-1,3,5-triene (DPH) was used for monitoring structural perturbations induced by lipopolysaccharide (LPS) of Escherichia coli (0111:B4) in plasma membranes of rat liver. Changes in microviscosity were observed in plasma membrane preparations from control rats after treatment with LPS and in plasma membrane preparations from liver perfused with LPS. In both systems fluorescence polarization was measured from which microviscosity was calculated. This parameter increases with LPS treatment. From temperature dependence studies was inferred that LPS interaction with plasma membrane preparations induces an increase of both the polarization term (r0/r-1)-1 and flow activation energy (delta E). Addition of LPS to hepatocyte suspensions also induces an increase on microviscosity and a delay in the fall of microviscosity induced by a temperature rise in hepatocyte monolayers grown on microcover slides. These data suggest that LPS interaction can be attributed to its binding to membrane hydrophobic regions in a non-specific manner.
荧光探针1,6 - 二苯基己三烯（DPH）用于监测大肠杆菌（0111:B4）脂多糖（LPS）诱导的大鼠肝脏质膜结构扰动。在用LPS处理的对照大鼠的质膜制剂以及用LPS灌注肝脏的质膜制剂中观察到微粘度的变化。在这两个系统中都测量了荧光偏振，并据此计算微粘度。该参数随LPS处理而增加。从温度依赖性研究推断，LPS与质膜制剂的相互作用导致偏振项（r0/r - 1）- 1和流动活化能（δE）均增加。向肝细胞悬液中添加LPS也会导致微粘度增加，并延迟在微盖玻片上生长的肝细胞单层中温度升高所诱导的微粘度下降。这些数据表明，LPS的相互作用可归因于其以非特异性方式与膜疏水区域结合。
