顺磁探针16－NS和荧光探针DPH在DPPG交插脂双层中的行为研究

研究了１６—ＮＳ和ＤＰＨ在被山莨菪碱诱导形成交插脂结构的ＤＰＰＧ脂质体中的行为。在交插脂双层结构中,标记在脂酰链末端的１６—ＮＳ的序参数明显增大,即同标记在靠脂酰链头部的５—ＮＳ的序参数的差距缩小。这些颇磁探针在交插脂双层结构中的运动比在非交插脂双层结构中受到更大的限制。ＤＰＨ荧光强度在ＤＰＰＧ由非交插脂双层转变为交插脂双层结构时急剧下降。引起这种下降的原因可能是膜脂在从非交插脂双层结构向交插脂双层结构的转变过程中使得ＤＰＨ处于一个更为亲水的环境中。     

山莨菪碱诱导DPPG／DPPC混合物形成交插凝胶相──荧光偏振研究

山莨菪碱诱导ＤＰＰＧ脂质体交插结构,其脂酰链末端插到对面分子层脂酰链第五个碳原子的位置,而生物膜中普遍存在的ＤＰＰＣ不能被山莨菪碱诱导形成交插相,但ＤＰＰＧ／ＤＰＰＣ混合物则能形成交插相,即伴随ＤＰＰＧ的交插,ＤＰＰＣ分子也发生交插。当ＤＰＰＧ／ＤＰＰＣ摩尔比为２：１或１：１时,其脂酰链末端插到对面分子层第八个碳原子的位置。当ＤＰＰＧ／ＤＰＰＣ摩尔比为１：２时,就不能发生交插而呈完全的非交插状态。同时,发现当体系中钠离子浓度达到４００ｍｍｏｌ／Ｌ时,山莨菪碱就不能再诱导ＤＰＰＧ形成交插凝胶相。     

膜脂的物理状态对G_s激活AC的影响

用生物膜的拆离与重建方法将从牛脑皮层膜中纯化的激活型ＧＴＰ结合蛋白（Ｇｓ）和腺苷酸环化酶（ＡＣ）在含有不同极性头部或不同脂肪酸侧链的磷脂组成的脂质体上重建形成脂酶体,测定脂酶体中ＡＣ的基础活力及Ｇｓ激活ＡＣ的活力。实验结果表明,磷脂影响ＡＣ的基础活力和Ｇｓ激活ＡＣ活力的顺序依次为：ＰＥ＞ＰＳ＞ＰＣ;含不同脂肪酸侧链的混合磷脂对Ｇｓ的激活活力的影响大于含单一脂肪酸侧链的纯磷脂,如ＰＥＤＰＰＥ,ＰＳＤＰＰＳ,ＰＣＤＰＰＣ。含不同脂肪酸侧链的磷脂影响Ｇｓ的活力的顺序为ＤＬＰＣ＞ＤＭＰＣ＞ＤＰＰＣ。用反映磷脂分子的堆积程度的荧光探剂ＭＣ５４０和脂双层的流动性变化的ＤＰＨ以及专一性标记蛋白质巯基（－ＳＨ）基团的荧光探剂ａｃｒｙｌｏｄａｎ的测定结果表明,不同磷脂影响Ｇｓ的活力的差异主要是由于脂质物理状态的不同所致。     

溶血磷脂对磷脂脂质体行为和结构的影响

利用差示量热扫描、荧光标记和X-射线衍射法测定了16:0溶血磷脂酰胆碱(LPC)、二棕榈酰磷脂酰胆碱(DPPC)混合脂质体的物化性质:脂双层相变温度、相变热熔、荧光偏振度、双层脂酰链的厚度,证明含有摩尔分数为14.1%和27.0%LPC的DPPC脂质体可以被LPC诱导呈交插脂双层结构,而交插的深度是LPC浓度的函数,当含量超过摩尔分数为30%LPC,混合脂质体趋向于微团化,脂双层膜结构逐渐被破坏,直至最后形成微团结构.     

牛胰多肽与脂作用时插膜状态的研究

利用单层膜和荧光技术,研究牛胰多肽（ＢＰＰ）和磷脂单分子层及脂质体的相互作用。ＢＰＰ与磷脂单分子层作用的动力学曲线以及临界插膜压表明它和磷脂,尤其是酸性磷脂有较强的相互作用;荧光研究表明,与脂作用后多肽内源性荧光光谱峰位蓝移,说明发荧光的酪氨酸残基存在由亲水环境向疏水环境的转变。荧光猝灭实验表明多肽与脂作用后,其内源性酪氨酸残基荧光更不容易被碘盐所猝灭,提示酪氨酸残基受到了脂双层的屏蔽作用;自旋标记磷脂的猝灭实验计算结果表明ＢＰＰ插膜深度在磷脂头部与脂酰链交界处稍内侧     

国人睾丸、附睾和输精管的氧化还原酶的组织化学观察

本文收集了１９—３８岁国人正常男性新鲜睾丸、附睾和输精管１３例,进行了氧化还原酶组织化学染色、光镜定位及定性观察。结果表明：睾丸曲细精管和输出小管上皮的ＧＤＨ,ＮＡＤＨＤ,ＮＡＤＰＨＤ,ＳＤＨ,ＧＰＤＨ,ＩＣＤＨ,ＭＤＨ,ＬＤＨ和Ｇ－６－ＰＤＨ９种酶;睾丸间质细胞和附睾管上皮的ＮＡＤＨＤ,ＮＡＤＰＨＤ,ＳＤＨ,ＩＣＤＨ,ＭＤＨ,ＧＤＨ,ＬＤＨ和Ｇ－６－ＰＤＨ８种酶;输精管的ＮＡＤＨＤ,ＮＡＤＰＨＤ,ＩＣＤＨ和ＧＤＨ４种酶的酶活性呈强阳性或极强阳性。提示输出小管和头部附睾管含有的多种氧化还原酶对精子功能成熟有极重要作用。     

磷脂模型膜的时间分辨纳秒荧光光谱的研究

叙述了用时间分辨率纳秒荧光技术研究大豆磷脂或合成磷脂模型膜（脂质体）的物理状态变化与荧光寿命以及时间分辨各向异性测量参数变化相关性的实验结果。用荧光探剂ＭＣ５４０标记模型膜的结果表明,荧光寿命（τ）的变化与脂质／探剂比例、磷脂组成、磷脂的极性头部、脂肪酸酰链长度等有关。用ＤＰＨ（１,６－ｄｉｐｈｅｎｙｌ－１,３,５－ｈｅｘａｔｒｉｅｎｅ）标记磷脂模型膜的时间分辨各向异性分析结果表明,序参数（Ｓ）、     

鸭肝脂肪酸合成酶的NADPH底物抑制及作用动力学

己知动物脂肪酸合成酶的底物乙酰辅酶Ａ和丙二酰辅酶Ａ具有竞争性双底物抑制的乒乓机制。实验发现鸭肝脂肪酸合成酶的第三个底物ＮＡＤＰＨ也具有底物抑制,并研究了它的规律及与ＮＡＤＰＨ有关的稳态动力学。发现对于该酶的全反应,增加丙二酰辅酶Ａ浓度,降低环境盐浓度,均使ＮＡＤＰＨ底物抑制减少。但以ＮＡＤＰＨ作底物的酮酰还原和烯酰还原二步单独反应以及包含四步单独反应的乙酰乙酰辅酶Ａ还原反应都无ＮＡＤＰＨ底物抑制现象。ＮＡＤＰＨ底物抑制对丙二酰辅酶Ａ为竞争性,丙二酰辅酶Ａ底物抑制对ＮＡＤＰＨ为非竞争性。在全反应中ＮＡＤＰＨ和丙二酰辅酶Ａ之间发现为乒乓机制,在乙酰乙酰辅酶Ａ还原反应中,两个底物ＮＡＤＰＨ和乙酰乙酰辅酶Ａ之间则表现为序列反应机制。降低环境盐浓度使ＮＡＤＰＨ和丙二酰辅酶Ａ之间的乒乓机制向序列机制转化。在全反应中,ＮＡＤＰ产物抑制相对ＮＡＤＰ为竞争性,对丙二酰辅酶Ａ为非竞争性。     

逆转录病毒载体介导诱导型NO合酶在神经细胞中表达

为了深入研究诱导型一氧化氮合酶基因表达产物在阿片耐受和依赖中作用,采用脂质体介导基因转染技术,将ｉＮＯＳ ｃＤＮＡ重组逆转录病毒载体导入ＮＧ１０８－１５神经细胞,获得Ｇ４１８抗性克隆,命名为ＮＧ－ＬＮＣＸｉＮＯＳ细胞。ＤＮＡ印迹杂交,ＰＣＲ扩增及ＲＴ－ＰＣＲ和蛋白质免疫印迹杂交分析,证实ＮＧ－ＬＮＣＸｉＮＯＳ细胞有外源ｉＮＯＳ基因整合,转录和表达;ＮＡＤＰＨ黄递酶（ＮＡＤＰＨ ｄｉａｐｈｏｒａｓｅ     

非诱导光周期对牵牛开花的抑制作用（简报）

非诱导光周期对牵牛开花的抑制作用（简报）范国强,谭克辉（中国科学院植物研究所,北京１０００４４）ＴＨＥＩＮＨＩＢＩＴＯＲＹＥＦＦＥＣＴＯＦＮＯＮ－ＩＮＤＵＣＥＤＰＨＯＴＯＰＥＲＩＯＤＯＮＴＨＥＦＬＯＷＥＲＩＮＧＯＦＰＨＡＲＢＩＴＩＳＮＩＬ￥ＦａｎＧｕ...     

二价金属离子对嵌有线粒体H~+-ATP酶的脂酶体不同层次脂质流动性的影响

本文报道用荧光偏振及顺磁共振两种方法研究Mg~(2+)及其它二价金属离子对嵌有H~+-ATP酶的脂酶体不同层次脂质流动性的影响。 (1)顺磁标记探剂5-、12-、16-氮氧基硬脂酸测定结果表明Mg~(2+)和其它二价金属离子都能降低膜脂双分子层表层的流动性。降低流动性的顺序为Mg~(2+)=Ca~(2+)>Sr~(2+)>Cd~(2+)。较深层脂则无明显变化。 (2)荧光探剂7-、12-(9-蒽酰)硬脂酸及16-(9-蒽酰)棕榈酸的测定结果也表明Mg~(2+)和其它二价金属离子降低了膜脂表层的流动性,尤以Mn~(2+)、Ca~(2+)降低流动性最显著,流动性降低的顺序为;Mn~(2+) Ca>Sr~(2+) Mg~(2+) Cd~(2+)。除Mn~(2+)、Ca~(2+)还能影响膜脂深层的流动性外,其它与对照无明显差异。     

Comparison of Membrane Pluidity of Seedling Mitochondria of Chilling Sensitive and Chilling Tolerant Rice

The membrane fluidity of seedling mitochondria of chilling-sensitive rice and that of chilling-tolerant rice were compared by using spin labeled stearic acid: 5, 12 16-NS and fluorescent probe DPH. From the ESR spectra using 5-NS as a spin labeled probe it clearly showed that the calculated order parameter (S) of seedling mitochondria of chilling-sensitive rice Qiu Guang was obviously higher than that of chilling-resistant rice Ji Geng 44. Similar results were obtained when seedling'mitochondria of another species of chilling sensitive Zao Jin were compared with those of chilling tolerant rice Ji Geng 60. Moreover, the difference of order parameters between Ji Geng 44 and Ji Geng 60 was quite small, but both of them are obviously lower than those of chilling-sensitive rice Qiu Guang or Zao Jin. The results using spin labeled probe 12-NS, 16-NS clearly showed that the relative correlation times (τc) of seedling mitochondria of chilling-sensitive rice Qiu Guang or Zao Jin was markedly higher than that of the chilling tolerant rice Ji Geng 44 or Ji Geng 60. A comparison of membrane fluidity of seedling mitochondria of chilling-sensitive and chilling-resistant rice using fluorescent probe DPH was also carried out. Similar results were obtained and showed that the fluidity of mitochondrial membrane of chilling resistant rice seedling was obviously higher than that of the chilling-sensitive ones. Thus, it seemed that the fluidity of mitochondrial membrane might be used as a biophysical test for screening chilling tolerance of rice at seedling stage.     

Interdigitation of phosphatidylcholine and phosphatidylethanolamine mixed with complexes of acidic lipids and polymyxin B or polymyxin B nonapeptide

A fatty acid spin label, 16-doxyl-stearic acid, was used to determine the percent interdigitated lipid in mixtures of a neutral phospholipid and an acidic phospholipid. Interdigitation of the acidic lipid was induced with polymyxin B (PMB) at a mole ratio of PMB to acidic lipid of 1:5. This compound does not bind significantly to neutral lipids or induce interdigitation of the neutral lipids by themselves. The neutral lipids used were dimyristoylphosphatidylcholine (DMPC), dipalmitoylphosphatidylcholine (DPPC), or dipalmitoylphosphatidylethanolamine (DPPE), and the acidic lipids were dipalmitoylphosphatidylglycerol (DPPG) or dipalmitoylphosphatidic acid (DPPA). The percent interdigitated lipid was determined from the percent of the spin label which is motionally restricted, assuming that the spin label is homogeneously distributed in the lipid. Assuming further that 100% of the acidic lipid is interdigitated at this saturating concentration of PMB, the percentage of the neutral lipid which can become interdigitated along with it was calculated. The results indicate that about 20 mole % DPPC can be incorporated into and become interdigitated in the interdigitated bilayer of PMB/DPPG at 4 degrees C. As the temperature approaches the phase transition temperature, the lipid becomes progressively less interdigitated; this occurs to a greater degree for the mixtures than for the single acidic lipid. Thus the presence of DPPC promotes transformation of the acidic lipid to a non-interdigitated bilayer at higher temperatures. At the temperature of the lipid phase transition little or none of the lipid in the mixture is interdigitated. Thus the lipid phase transition detected by calorimetry is not that of the interdigitated bilayer. The shorter chain length DMPC can be incorporated to a greater extent than DPPC, 30-50 mol%, in the interdigitated bilayer of PMB-DPPG. This may be a result of reduced exposure of the terminal methyl groups of the shorter myristoyl chains at the polar/apolar interface of the interdigitated bilayer. Less than 29% of the total lipid was interdigitated in a DPPC/DPPA/PMB 1:1:0.2 mixture indicating that none of the DPPC in this mixture becomes interdigitated. This is attributed to the lateral interlipid hydrogen bonding interactions of DPPA which inhibits formation of an interdigitated bilayer. DPPE was found to be incorporated into the interdigitated bilayer of PMB-DPPG to a similar extent as DPPC if the amount of PMB added is sufficient to bind to only the DPPG in the mixture. Differential scanning calorimetry showed that the remaining non-interdigitated DPPE-enriched mixture phase separates into its own domain.(ABSTRACT TRUNCATED AT 400 WORDS)     

Electron spin resonance investigation of the interaction of the anion and glucose transport inhibitor, p-azidobenzylphlorizin, with the human red cell membrane

The membrane perturbations caused by the interaction of p-azidobenzylphlorizin (p-AzBPhz), a potential photoaffinity labeling agent of the anion and D-glucose transporters in the human erythrocyte, have been studied using electron spin resonance (ESR) spectrometry. Two lipid-specific spin labels have been employed; one of these agents, a hexadecyl-quarternary amine with the nitroxide reporter group covalently attached to the cationic nitrogen, (CAT-16), has been used to monitor changes in the physical state of the membrane's extracellular phospholipid/water interface. The other spin label, 5-doxylstearic acid (5-NS), is designed to examine the order and motion of the lipid bilayer near the cell surface. In separate experiments, intact human red cells labeled with these lipid-specific spin labels were exposed to small amounts of the phlorizin azide. A dose-dependent alteration in CAT-16 motion was observed, but the p-AzBPhz interaction with the membrane had no effect on the spectrum of 5-NS. The half-maximal effect of the phlorizin derivative on the CAT-16 spectrum occurred when about 2 million molecules were bound to each cell. This is also the combined amount of band 3 and band 4.5 present in the red cell membrane and represents the concentration necessary to inhibit both anion and glucose transport. Our results suggest that the first p-AzBPhz molecules binding to the red cell membrane interact with the anion and sugar transporters, and not with the bulk lipid bilayer.     

Abnormal fluidity state in membranes of malignant hyperthermia pig skeletal muscle

The fluidity state was analyzed on sarcoplasmic reticulum membranes and phospholipid vesicles prepared from normal and malignant hyperthermia susceptible pig muscle. Electron spin resonance studies were performed to determine the fluidity state at the region near the polar headgroups and in the central core of the bilayer using 5-nitroxide (5-NS) and 16-nitroxide stearic acid (16-NS), respectively. With the 5-NS label, no differences were found between normal and malignant hyperthermia sarcoplasmic reticulum (MH SR) membranes whereas with the 16-NS label, a significant increase of the activation energy was shown with MH membranes. Lower values of fluorescence anisotropy observed with DPH-labeled MH membranes as compared with normal ones, confirmed the higher abnormal fluidity state of these membranes. The fluidizing effect of halothane, a triggering agent of malignant hyperthermia syndrome, was also studied in these membranes. We show that a relatively low concentration of the drug destabilized not only the diseased sarcoplasmic reticulum membranes but also the vesicles made of total phospholipids extracted from MH skeletal muscle. Together, these findings strongly suggest that an overall increase in membrane fluidity may be implied in the MH disease, improving the general membrane defect hypothesis for this syndrome.     

Site-specific mechanisms of initiation by chelated iron and inhibition by alpha-tocopherol of lipid peroxide-dependent lipid peroxidation in charged micelles.

To obtain information on the role of iron-catalyzed lipid peroxidation in the presence of the small amount of lipid peroxide in deterioration of biological membranes, we examined factors affecting peroxidation of fatty acids in charged micelles. Peroxidation of linoleic acid (LA) was catalyzed by Fe2+ via reductive cleavage of linoleic acid hydroperoxide (LOOH) in negatively charged sodium dodecyl sulfate micelles, but not in positively charged tetradecyltrimethylammonium bromide (TTAB) micelles. However, this Fe2(+)-induced, LOOH-dependent lipid peroxidation could be induced in TTAB micelles in the presence of a negatively charged iron chelator, nitrilotriacetic acid (NTA). The linoleic acid alkoxy radical (LO.) generated by the LOOH-dependent Fenton reaction was also trapped by N-t-butyl-alpha-phenylnitrone at the surface of TTAB micelles in the presence of NTA, but not in its absence. The degradation rates of two spin probes, N-oxyl-4,4'-dimethyloxazolidine derivatives of stearic acid (5-NS and 16-NS), were investigated to determine the site of production of radicals formed during LOOH-dependent lipid peroxidation. The rate of consumption of 16-NS during the LOOH-dependent Fenton-like reaction was higher in TTAB micelles containing LA than in those containing lauric acid (LauA), although the rates of formation of LO. in the two types of fatty acid micelles were similar. The rates of 5-NS consumption in LA and LauA micelles were almost the same and were as low as that of 16-NS consumption in LauA micelles. 16-NS was more inhibitory than 5-NS of LOOH-dependent lipid peroxidation, and this inhibition was associated with its higher consumption of 16-NS than of 5-NS. alpha-Tocopherol inhibited NTA-Fe2(+)-induced LOOH-dependent lipid peroxidation in TTAB micelles, and was oxidized during this inhibition process. The rate and amount of alpha-tocopherol oxidized by the LOOH-dependent Fenton reaction were higher in LA micelles than in LauA micelles. alpha-Tocopherol inhibited the consumption of 16-NS during NTA-Fe2(+)-induced LOOH-dependent lipid peroxidation more effectively than that of 5-NS. The distribution of the chromanol moiety of alpha-tocopherol was studied by the fluorescence quenching method. There was no difference between Stern-Volmer plots of the quenchings of alpha-tocopherol fluorescence by 5-NS and 16-NS. From these results, we discuss the mechanism of induction of LOOH-dependent peroxidation of LA and the mechanism of the antioxidant effects of alpha-tocopherol on it from the viewpoint of site-specific reaction.     

Penetration of an emulsion surface by cholesteryl ester transfer protein

Quenching of the intrinsic fluorescence of cholesteryl ester transfer protein (CETP) by spin labelled fatty acids (5-NS and 16-NS) was investigated to determine the degree to which the protein penetrated the phospholipid monolayer surface of a lipid emulsion. When bound to the phospholipid surface approximately 50% of the fluorophores of the transfer protein were accessible to quenching by 5-NS whose nitroxy group locates near the monolayer surface. On the other hand, only 22% of the fluorophores of CETP were accessible to quenching by 16-NS whose nitroxy group locates deeper in the surface monolayer. Quenching of the CETP fluorescence by an aqueous phase quencher (acrylamide) shows that the protein undergoes a conformational change on binding which increases the proportion of the tryptophan residues exposed to the aqueous phase. The results indicate that CETP does not penetrate the lipid surface to a significant degree. Received: 29 March 1996 / Accepted: 30 May 1996     

Effect of acylation on the interaction of the N-Terminal segment of pulmonary surfactant protein SP-C with phospholipid membranes

SP-C, the smallest pulmonary surfactant protein, is required for the formation and stability of surface-active films at the air-liquid interface in the lung. The protein consists of a hydrophobic transmembrane α-helix and a cationic N-terminal segment containing palmitoylated cysteines. Recent evidence suggests that the N-terminal segment is of critical importance for SP-C function. In the present work, the role of palmitoylation in modulating the lipid-protein interactions of the N-terminal segment of SP-C has been studied by analyzing the effect of palmitoylated and non-palmitoylated synthetic peptides designed to mimic the N-terminal segment on the dynamic properties of phospholipid bilayers, recorded by spin-label electron spin resonance (ESR) spectroscopy. Both palmitoylated and non-palmitoylated peptides decrease the mobility of phosphatidylcholine (5-PCSL) and phosphatidylglycerol (5-PGSL) spin probes in dipalmitoylphosphatidylcholine (DPPC) or dipalmitoylphosphatidylglycerol (DPPG) bilayers. In zwitterionic DPPC membranes, both peptides have a greater effect at temperatures below than above the main gel-to-liquid-crystalline phase transition, the palmitoylated peptide inducing greater immobilisation of the lipid than does the non-palmitoylated form. In anionic DPPG membranes, both palmitoylated and non-palmitoylated peptides have similar immobilizing effects, probably dominated by electrostatic interactions. Both palmitoylated and non-palmitoylated peptides have effects comparable to whole native SP-C, as regards improving the gel phase solubility of phospholipid spin probes and increasing the polarity of the bilayer surface monitored by pK shifts of fatty acid spin probes. This indicates that a significant part of the perturbing properties of SP-C in phospholipid bilayers is mediated by interactions of the N-terminal segment. The effect of SP-C N-terminal peptides on the chain flexibility gradient of DPPC and DPPG bilayers is consistent with the existence of a peptide-promoted interdigitated phase at temperatures below the main gel-to-liquid-crystalline phase transition. The palmitoylated peptide, but not the non-palmitoylated version, is able to stably segregate interdigitated and non-interdigitated populations of phospholipids in DPPC bilayers. This feature suggests that the palmitoylated N-terminal segment stabilizes ordered domains such as those containing interdigitated lipids. We propose that palmitoylation may be important to promote and facilitate association of SP-C and SP-C-containing membranes with ordered lipid structures such as those potentially existing in highly compressed states of the interfacial surfactant film.     

Use of spin labels to determine the percentage of interdigitated lipid in complexes with polymyxin B and polymyxin B nonapeptide

Long chain spin labels with the nitroxide group located near the terminal methyl of the chain were used to determine the percentage interdigitated lipid in complexes of polymyxin B (PMB) and polymyxin B nonapeptide (PMBN) with the acidic lipids dipalmitoylphosphatidylglycerol (DPPG) and dipalmitoylphosphatidic acid (DPPA) at varying mole ratios of drug to lipid and at different pH values. These spin labels are more motionally restricted in the interdigitated than in the non-interdigitated gel phase bilayer. This allows determination of the percentage interdigitated lipid by resolution of the spectrum into motionally restricted and more mobile components. At nonsaturating concentrations of PMB, significantly more DPPG than that which can be maximally PMB-bound, becomes interdigitated. As the temperature approaches the gel to liquid crystalline phase transition temperature, the bilayer becomes progressively non-interdigitated. The ESR spectrum indicates that PMB also causes interdigitation of DPPA. However, in contrast to DPPG, the amount of DPPA which is interdigitated at pH 6, is less than the amount which is expected to be PMB-bound. This is attributed to the ability of DPPA to participate in lateral interlipid hydrogen bonding interactions. Such lateral interactions would be abolished in the interdigitated bilayer and thus they are expected to inhibit its formation. At pH 9, where the interlipid interactions of DPPA are weakened, PMB induces even more lipid than that which is PMB-bound to become interdigitated. Indeed, the percentage interdigitated lipid is even greater than found for DPPG. This may be partly a result of the greater negative charge of DPPA at this pH. A greater repulsive negative charge is expected to favor interdigitation. PMBN is less effective than PMB at inducing interdigitation of DPPG and causes little or no interdigitation of DPPA at pH 6, even at saturating concentrations. PMBN also does not lower the phase transition temperature of DPPA at pH 6 as much as PMB. At pH 9, the effect of PMBN on DPPA is more similar to the effect of PMB. However, even for DPPG, and DPPA at pH 9, PMBN does not maintain interdigitation of the lipids at higher temperatures as effectively as PMB. PMBN's smaller perturbing effect and greatly decreased ability to cause interdigitation of DPPA at pH values below 9 may be related to a decreased ability to cause lateral separation of the lipid molecules, which is necessary in order to weaken the interlipid interactions.(ABSTRACT TRUNCATED AT 400 WORDS)