Morimoto Y, Hosokawa M, Sayo H, Takeuchi Y
Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Kobe-Gakuin University, Japan.
Chem Pharm Bull (Tokyo). 1994 Jan;42(1):123-9. doi: 10.1248/cpb.42.123.
The mechanism of interaction between chlorpromazine (CPZ) and artificial lipid membranes, negatively or positively charged liposomes was studied by an electron spin resonance (ESR) technique. Analysis by a 5-doxyl stearic acid (DS) spin probe indicated that regardless of the electric charge of liposomes, CPZ disordered the hydrophobic region near the surface of lipid membranes at CPZ/lipid > 1. In the same CPZ/lipid range, the lysis of liposomes was observed, and it was considered that the formation of the CPZ/lipid mixed micelles as a consequence of this collapse of liposomes would probably lead to the disordering of the 5-DS reporting region. As to the middle portion of the fatty acyl chains reported by the 12-DS spin probe, the membrane disordering action of CPZ was only detected with the negatively charged liposomes at a ratio of CPZ/lipid < 1, but no membrane alteration was observed with the positively charged liposomes, regardless of the concentration range of CPZ used. In comparing these two opposite results, it is conceivable that the disordering at the 12-DS reporting region was probably induced by the cationized CPZ which would enter into the hydrocarbon-polar interface, leading to an expansion of the space between the hydrocarbon chains at this area. Also, a strong influence of CPZ on the innermost portion of the lipid bilayers was observed with both the negatively and positively charged liposomes, as reported by the 16-DS probe. This perturbing action presumably occurred when undissociated CPZ molecules penetrated into the center of the bilayers (lipid core), which could have resulted in a reduction of hydrophobic interactions of the lipid molecules.
采用电子自旋共振(ESR)技术研究了氯丙嗪(CPZ)与人工脂质膜、带负电或正电脂质体之间的相互作用机制。用5-硬脂酸多氧自由基(DS)自旋探针分析表明,无论脂质体的电荷如何,当CPZ/脂质>1时,CPZ会使脂质膜表面附近的疏水区域无序化。在相同的CPZ/脂质范围内,观察到脂质体的裂解,并且认为脂质体这种塌陷导致的CPZ/脂质混合胶束的形成可能会导致5-DS报告区域的无序化。对于由12-DS自旋探针报告的脂肪酰链中间部分,仅在CPZ/脂质<1的比例下,带负电的脂质体检测到CPZ的膜无序化作用,但无论使用的CPZ浓度范围如何,带正电的脂质体均未观察到膜改变。在比较这两个相反的结果时,可以想象12-DS报告区域的无序化可能是由阳离子化的CPZ引起的,阳离子化的CPZ会进入烃-极性界面,导致该区域烃链之间的空间扩大。此外,如16-DS探针所报告的,带负电和正电脂质体均观察到CPZ对脂质双层最内层有强烈影响。这种扰动作用可能发生在未离解的CPZ分子渗透到双层中心(脂质核心)时,这可能导致脂质分子疏水相互作用的减少。