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Potentiation of oxygen-induced lung injury in rats by the mechanism-based cytochrome P-450 inhibitor, 1-aminobenzotriazole

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期292卷 553-560页

作者： Moorthy, B Parker, KM Smith, CV Bend, JR Welty, SE Baylor Coll Med Dept Pediat Houston TX 77030 USA Univ Western Ontario Dept Pharmacol & Toxicol London ON Canada

In this investigation, we tested the hypothesis that the cytochrome P-450 (CYP) inhibitor 1-aminobenzotriazole (ABT) alters the susceptibility of rats to hyperoxic lung injury. Male Sprague-Dawley rats were treated i.p. with ABT (66 mg/kg), i.v. with N-benzyl-1-aminobenzotriazole (1 mmol/kg), or the respective vehicles, followed by exposure to >95% oxygen for 24, 48, or 60 h. Pleural effusion volumes were measured as estimates of hyperoxic lung injury, and lung microsomal ethoxyresorufin O-deethylation (EROD) (CYP1A1) activities and CYP1A1 apoprotein levels were determined by Western blotting. ABT-pretreated animals exposed to hyperoxia died between 48 and 60 h, whereas no deaths were observed with up to 60 h of hyperoxia in vehicle-treated animals. In addition, three of four ABT-treated rats exposed to hyperoxia for 48 h showed marked pleural effusions. Exposure of vehicle-treated rats to hyperoxia led to 6.3-fold greater lung EROD activities and greater CYP1A1 apoprotein levels than in air-breathing controls after 48 h, but both declined to control levels by 60 h. Liver CYP1A1/1A2 enzymes displayed responses to hyperoxia and ABT similar to the effects on lung CYP1A1. N-Benzyl-1-aminobenzotriazole markedly inhibited lung microsomal pentoxyresorufin O-depentylation (principally CYP2B1) activities in air-breathing and hyperoxic animals but did not affect lung EROD or liver CYP activities. In conclusion, the results suggest that induction of CYP1A enzymes may serve as an adaptive response to hyperoxia, and that CYP2B1, the major pulmonary CYP isoform, does not contribute significantly to hyperoxic lung injury.

关键词：印迹法蛋白质细胞色素P450CYP1A1/代谢细胞色素P450CYP1A2/代谢细胞色素P450酶系统/拮抗剂和抑制剂药物协同作用酶抑制剂/药理学高氧症/死亡率高氧症/病理学肝/药物作用肝/酶学微粒体/药物作用微粒体/代谢恶嗪类/药代动力学氧/毒性胸腔积液蛋白质亚型/药理学大鼠 Sprague-Dawley 呼吸窘迫综合征成人/化学诱导呼吸窘迫综合征成人/死亡率时间因素三唑类/药理学动物男(雄)性大鼠

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Activation of acyl-CoA cholesterol acyltransferase:: Redistribution in microsomal fragments of cholesterol and its facilitated movement by methyl-β-cyclodextrin

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LIPIDS 1999年第3期34卷 261-268页

作者： Cheng, DH Tipton, CL Iowa State Univ Dept Biochem & Biophys Ames IA 50011 USA

Acyl-CoA cholesterol acyltransferase (ACAT) (EC 2.3.1.26) in the yolk sac membrane of chicken eggs plays an important role in the transport of lipids, which serve as both structural components and as an energy source during embryogenesis. ACAT from the yolk sac membrane of chicken eggs 16 d after fertilization has higher activity and better stability than its mammalian liver counterpart. During our study of the avian enzyme, ACAT was round to be activated up to twofold during storage at 4 degrees C. The activation was investigated, and data suggest that redistribution of cholesterol within microsomal vesicles leads to the increase. Methyl-beta-cyclodextrin (M beta CD) increases activation an additional twofold, possibly by facilitating the movement of cholesterol within microsomal fragments and allowing redistribution of cholesterol in lipid bilayers to a greater extent. Treatment of microsomes with M beta CD removes cholesterol from the membranes. Controlled amounts of cholesterol can be restored to the membranes by mixing them with cholesterol-phosphatidylcholine liposomes in the presence of M beta CD. Under these conditions, the plot of ACAT vs. cholesterol mole fraction in the liposomes is sigmoidal. The finding that M beta CD can enhance cholesterol transfer between liposomes and microsomes and reduce the limitation of slow movement of nonpolar molecules in aqueous media should make cyclodextrins more useful in in vitro studies of apolar molecule transport between membrane vesicles.

关键词：生物转运细胞膜/代谢鸡胆固醇/代谢低温保存环糊精类/药理学剂量效应关系药物蛋黄/代谢酶激活/药物作用脂双层微粒体/药物作用微粒体/代谢甾醇O-酰基转移酶/药物作用甾醇O-酰基转移酶/代谢 β环糊精类动物

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Monitoring mobility in the early steps of unfolding:: The case of oxidized cytochrome b₅ in the presence of 2 M guanidinium chloride

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BIOCHEMISTRY 2000年第24期39卷 7117-7130页

作者： Arnesano, F Banci, L Bertini, I Koulougliotis, D Monti, A Univ Florence CERM Sesto Fiorentino Italy Univ Florence Dept Chem Sesto Fiorentino Italy

A Model-Free analysis of the N-15 relaxation properties of oxidized cytochrome bs, a heme-containing electron-transfer protein, has been performed in 2 M guanidinium chloride (GdmCl), i.e., just before the heme is released by the action of denaturant. This analysis provides information on the mobility in the nano- to picosecond time range. A parallel study on the motions in the milli- to microsecond time scale has also been performed by analyzing rotating-frame N-15 relaxation rates. The protein contains a 60:40 ratio of two conformers (A and B) differing for the rotation of the heme group around the alpha-gamma meso axis. The effect of denaturant has been followed for both species, and the mobility properties have been compared with the analogous information in the absence of denaturant. To complete the picture, we also performed N-15 relaxation measurements and the Model-Free analysis of the native B form, whereas data on the A form [Dangi, B., Sarma, S., Yan, C., Banville, D. L., Guiles, R. D. (1998) J. Phys. Chem. B 102, 8201-8208], as well as rotating-frame measurements for both native forms [Banci, L., Bertini, I., Cavazza, C., Felli, I. C., Koulougliotis, D. (1998) Biochemistry 37, 12320-12330;Arnesano, F., Banci, L., Bertini, I., Felli, I. C., Koulougliotis, D. (1999) Eur. J. Biochem, 260, 347-354], are already available in the literature. It is found that GdmCl tends to increase the internal mobility, although some residues are rigidified on both time scales. In the milli- to microsecond time scale, the tendency to increased mobility is reflected in a decrease in the tau(ex) values rather than in the number of residues experiencing conformational equilibria. In the nano- to picosecond time scale, the tendency to increased mobility is indicated by an overall decrease in the S-2 values. Color pictures are reported to visually show these effects. On the fast time scale, the B form is more mobile than the A form, reflecting the different stability with respect

关键词：细胞色素b5类/化学胍/药理学血红素/化学动力学磁共振波谱学微粒体/药物作用微粒体/酶学模型分子氮同位素蛋白质构象/药物作用蛋白质变性蛋白质折叠动物大鼠

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Electrostatic interaction between cytochrome P450 and NADPH-P450 reductase: Comparison of mixed and fused systems consisting of rat cytochrome P4501A1 and yeast NADPH-P450 reductase

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第2期257卷 273-278页

作者： Kondo, S Sakaki, T Ohkawa, H Inouye, K Kyoto Univ Grad Sch Agr Div Appl Life Sci Sakyo Ku Kyoto 6068502 Japan Kobe Univ Fac Agr Dept Biol & Environm Sci Nada Ku Kobe Hyogo 6570013 Japan

The electrostatic interaction between rat cytochrome P450 1A1 and yeast NADPH-P450 reductase was analyzed by using recombinant yeast microsomes containing both native enzymes or their fused enzyme. The V-max of the 7-ethoxycoumarin O-deethylation in the recombinant microsomes containing both rat cytochrome P4501A1 and yeast NADPH-P450 reductase (the mixed system) was maximal when the ionic strength of the reaction mixture was 0.1-0.15, However, on the fused enzyme between rat cytochrome P450 1A1 and yeast NADPH-P450 reductase (the fused system), the activity was uniformly reduced with increasing ionic strength. The pH profiles of V-max were also different between the mixed and the fused systems. Based on these results, we propose a hypothesis that cytochrome P450 and NADPH-P450 reductase have more than one binding mode. The maximal activity of the mixed system at ionic strength of 0.1-0.15 is explained by change of the binding mode. On the other hand, the fused enzyme appears to have only one binding mode due to the limited topology of cytochrome P450 and NADPH-P450 reductase domains. (C) 1999 Academic Press.

关键词：催化作用/药物作用香豆素类/代谢细胞色素P450酶系统/化学细胞色素P450酶系统/遗传学细胞色素P450酶系统/代谢静电学氢离子浓度动力学微粒体/药物作用微粒体/代谢 NADH NADPH氧化还原酶类/化学 NADH NADPH氧化还原酶类/遗传学 NADH NADPH氧化还原酶类/代谢 NADPH高铁血红素蛋白还原酶容积渗克分子浓度氧化还原/药物作用氯化钾/药理学蛋白质结合蛋白质构象重组融合蛋白质类/化学重组融合蛋白质类/遗传学重组融合蛋白质类/代谢酵母菌酿酒/酶学酵母菌酿酒/遗传学氯化钠/药理学动物大鼠

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Effect of low-level short-term o-xylene inhalation on benzo[a]pyrene (BaP) metabolism and BaP-DNA adduct formation in rat liver and lung microsomes

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JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A 1999年第5期58卷 299-312页

作者： Park, SH Schatz, RA Northeastern Univ Toxicol Program Boston MA 02115 USA

o-Xylene is a commonly used solvent that alters mixed-function oxidase (MFO) activity in an organ- and isozyme-specific pattern following intraperitoneal tip) administration. Similar MFO alterations have been observed after ip or inhalation exposure to other methyl benzenes. These MFO alterations shifted the metabolism of the carcinogen benzo[a]pyrene (BaP) toward formation of toxication metabolites in lung. The purpose of this study was to determine whether o-xylene inhalation caused similar MFO changes and whether these alterations were reflected in altered BaP metabolism and BaP-DNA adduct formation. o-Xylene (300 ppm;6 h) decreased the activity of arylhydrocarbon hydroxylase (AHH) in lung. CYP2B1 activity (benzyloxyresorufin O-dealkylase;BROD), which is responsible for metabolism of BaP to relatively nontoxic metabolites, was decreased in lung, as was, to a lesser extent, CYP1A1 (ethoxyresorufin O-dealkylase;EROD), which is responsible for metabolism of BaP to reactive/toxic metabolites. The BROD/EROD ratio, an indirect indicator of the pattern of BaP toxication/detoxication, was decreased in lung, suggesting that BaP metabolism is shifted toward toxication. No MFO alterations were observed in liver. In lung microsomes, o-xylene increased formation of 7,8-BaP-diol, while 9,10-BaP-diol, 3-OH BaP, and 9-OH BaP were decreased. In liver, o-xylene increased 9-OH BaP formation, while 4,5- and 9,10-diols as well as total diets were decreased. The toxication/detoxication ratios for BaP individual and total metabolite groups were increased in lung microsomes and unaltered in liver. The major BaP-DNA adduct, BaP diet epoxide-N-2-deoxyguanosine, was increased in lung but decreased in liver microsomes from o-xylene-exposed rats. Four minor BaP-DNA adducts were formed in lung and three in liver, only one of which (liver adduct 3) was decreased. The o-xylene-induced increase in BaP adduct formation in lung and decrease in liver indicate that coexposure to organic solvents suc

关键词：投药吸入苯并芘/代谢生物转化致癌物/代谢色谱法气相色谱法高压液相细胞色素P450CYP1A1/代谢细胞色素P450CYP2B1/代谢 DNA加合物/代谢肺/药物作用肺/酶学肺/代谢微粒体/药物作用微粒体/酶学微粒体/代谢微粒体肝/药物作用微粒体肝/酶学微粒体肝/代谢混合功能氧化酶类/代谢二甲苯类/投药和剂量二甲苯类/血液二甲苯类/毒性动物大鼠

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Interactions between cytochrome P-450 activities and ozone-induced modulatory effects on endothelial permeability in rabbit lungs: Influence of gender

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INHALATION TOXICOLOGY 1999年第11期11卷 999-1014页

作者： Delaunois, A Florquin, S Segura, P Montano, LM Vargas, MH Gustin, P Univ Liege Dept Pharmacol Toxicol Fac Med Vet B-4000 Cointe Ougree Belgium Inst Nacl Enfermedades Resp Dept Invest Asthma Mexico City DF Mexico Univ Nacl Autonoma Mexico Fac Med Vet Dept Pharmacol Mexico City 04510 DF Mexico

The effects of rabbit exposure to ozone (O-3) (0.4 ppm for 4 h) on two different cytochrome P-450 (CYP450)-dependent activities were investigated. In turn, the role of CYP450 in the inhibitory effect of O-3 on acetylcholine (ACh)-evoked increase in endothelial permeability was also assessed. Immediately after the period of exposure, rabbits of both sexes were sacrificed and their lungs were extracted. Some lungs were used for preparation of microsomes and measurement of 7-ethoxyresorufin O-deethylase (EROD) and parathion oxidase activities. Other rabbit lungs were isolated and recirculatingly blood-free perfused. Arterial, venous pressures, and lung weight were continuously recorded. Capillary pressure was measured by applying the double occlusion method. Capillary filtration coefficient (K-f,K-c) was evaluated by measuring the amount of fluid filtering through the endothelium when vascular pressures were suddenly increased. Dose-response curves to ACh were constructed in air- or O-3-exposed rabbits. Some animals were pretreated with piperonyl butoxide (PBO), a well-known inhibitor of CYP450. O-3 significantly reduced both EROD and parathion oxidase lung microsomal activities in females, while it had no effect in males. Exposure to O-3 strongly inhibited the ACh-induced increase in K-f,K-c. Pretreatment with PBO reversed the modulatory effect of O-3 on endothelial permeability in male rabbits, but not in females. it was concluded (1) that inhibition of 2 different CYP450-dependent activities after exposure to 0.4 ppm O-3 for 4 h appears to be a gender-dependent phenomenon, and (2) that CYP450 is probably involved in the O-3-evoked inhibitory mechanism against ACh-induced increase in endothelial permeability, but only in males.

关键词：芳基二烷基磷酸酶毛细血管通透性/药物作用细胞色素P450CYP1A1/代谢细胞色素P450酶系统/拮抗剂和抑制剂细胞色素P450酶系统/代谢内皮/代谢内皮/病理学酶抑制剂/药理学酯酶类/代谢肺/酶学肺/病理学微粒体/药物作用微粒体/酶学氧化剂光化学/毒性臭氧/毒性胡椒基丁醚/药理学性征动物女(雌)性男(雄)性兔

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Constitutive and inducible cytochromes P450 in rat lung mitochondria: Xenobiotic induction, relative abundance, and catalytic properties

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TOXICOLOGY AND APPLIED PHARMACOLOGY 1999年第3期156卷 231-240页

作者： Bhagwat, SV Mullick, J Raza, H Avadhani, NG Univ Penn Sch Vet Med Dept Biol Anim Biochem Lab Philadelphia PA 19104 USA

The presence of xenobiotic-inducible CYP1A1, 2B1/2, and 3A1/2 in rat lung mitochondria was investigated using mitochondrial preparations of defined purity. The mitochondrial P450 content in uninduced lung was 1.5-fold higher compared to microsomes. Administration of BNF induced the P450 contents by twofold in both mitochondrial and microsomal membrane fractions. BNF treatment induced EROD activity to about 40-fold in the microsomal fraction and 25-fold in the mitochondrial fraction. The microsomal induction was observed at 4 days of BNF treatment, while the mitochondrial induction required 10 days of treatment. Consistent with the activity profile, Western blot analysis showed the presence of CYP1A1 antibody reactive protein only in lung mitochondria from BNF-treated rats. BNF administration also caused a 50 to 80% reduction in the CYP2B1/2-associated PROD and BROD activities and CYP3A1/2-associated ERND activity in both mitochondria and microsomes. There was also a parallel reduction in the antibody reactive CYP2B1/2 and 3A1/2 proteins in both of these membrane fractions. Administration of DEX for 4 days induced mitochondrial and microsomal ERND activity by 1.7- and 2.5-fold, respectively. Mitochondrial EROD activity was inhibited by antibodies to P450MT2, as well as Adx, but not by antibody against P450 reductase, indicating the :mitochondrial localization of CYP1A1. Protease protection and alkaline extraction experiments indicated that CYP1A1 associated with lung mitochondria is localized inside the inner membrane and exists as a membrane extrinsic protein. In summary, this is probably the first report of inducible P450s in rat lung mitochondria, and our results suggest a possible functional role for these mitochondrial enzymes in xenobiotic metabolism. (C) 1999 Academic Press.

关键词：芳基烃羟化酶类印迹法 RNA 催化作用细胞色素P450CYP1A1/生物合成细胞色素P450CYP2B1/生物合成细胞色素P450酶系统/生物合成酶诱导/药物作用同工酶类/生物合成肺/酶学膜蛋白质类/代谢微粒体/药物作用微粒体/酶学线粒体/酶学混合功能氧化酶类/生物合成大鼠 Sprague-Dawley 甾类羟化酶类/生物合成亚细胞部分/酶学异生物质/药理学动物男(雄)性大鼠

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Effects of the flavoprotein inhibitor, diphenyleneiodonium sulfate, on ex vivo organic nitrate tolerance in the rat

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期293卷 569-577页

作者： Ratz, JD McGuire, JJ Anderson, DJ Bennett, BM Queens Univ Fac Hlth Sci Dept Pharmacol & Toxicol Kingston ON K7L 3N6 Canada

The flavoprotein inhibitor, diphenyleneiodonium (DPI), inhibits the action of glyceryl trinitrate (GTN) and the D-enantiomer of isoidide dinitrate (IIDN), but not the L-enantiomer (L-IIDN), in isolated rat aorta via inhibition of the bioactivation of these prodrugs. Paradoxically, a vascular NAD(P)H oxidase, which also is inhibited by DPI, has been proposed to generate superoxide that quenches nitric oxide (NO) produced during GTN biotransformation, and increased oxidase levels are proposed to contribute to the phenomenon of organic nitrate tolerance. We examined the effect of DPI on isolated rat aorta using an in vivo model of organic nitrate tolerance. The EC50 values for GTN-, D-IIDN-, and L-IIDN-induced relaxation of aorta from GTN- tolerant rats were increased 4.5- to 7.5-fold. Treatment of blood vessels with DPI (0.3 mu M) increased the EC50 values for GTN and D-IIDN by the same magnitude in control and tolerant aortae, a result that would not be predicted if DPI and GTN tolerance affected common targets. The expression of NADPH-cytochrome P450 reductase (CPR) during in vivo tolerance was assessed by NADPH-dependent cytochrome c reductase activity of aortic microsomes, immunoblotting, and Northern analysis. By all three determinants, CPR expression was unchanged in aorta from GTN- tolerant rats. Superoxide dismutase-inhibitable NADPH-dependent cytochrome c reductase activity (a measure of superoxide generation) of tolerant rat aortic microsomes was not different from that of controls. Superoxide dismutase-inhibitable NADH-dependent cytochrome c reductase activity was detected only in microsomes from tolerant animals. DPI caused a modest increase in the sensitivity for relaxation by the NO donor DEA NONOate to an equal extent in tolerant and nontolerant tissues, whereas the superoxide scavenger, 4,5-dihydroxy-1,3-benzene disulfonic acid (Tiron), had no effect on the sensitivity for relaxation by GTN. These results would not be expected if tolerance-induced incr

关键词：主动脉胸/药物作用生物转化印迹法 RNA 药物耐受性酶抑制剂/药理学黄素蛋白类/拮抗剂和抑制剂谷胱甘肽/类似物和衍生物谷胱甘肽/药理学异山梨酯硝酸/拮抗剂和抑制剂异山梨酯硝酸/代谢异山梨酯硝酸/药理学微粒体/药物作用微粒体/代谢肌平滑血管/药物作用 NADPH高铁血红素蛋白还原酶/代谢硝酸盐类/拮抗剂和抑制剂硝酸盐类/代谢硝酸盐类/药理学一氧化氮供体/药理学一氧化氮合酶/拮抗剂和抑制剂硝酸甘油/拮抗剂和抑制剂硝酸甘油/代谢硝酸甘油/药理学亚硝基化合物/药理学鎓类化合物/药理学药物前体/代谢药物前体/药理学大鼠 Sprague-Dawley S-亚硝基谷胱甘肽立体异构现象超氧化物类/代谢血管舒张药/拮抗剂和抑制剂血管舒张药/代谢血管舒张药/药理学动物男(雄)性大鼠

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Reductions of nitro and 9-oxo groups of environmental nitrofluorenes by the rat mammary gland in vitro

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CHEMICAL RESEARCH IN TOXICOLOGY 2000年第8期13卷 793-800页

作者： Ritter, CL Decker, RW Malejka-Giganti, D Vet Affairs Med Ctr Minneapolis MN 55417 USA Univ Minnesota Dept Lab Med & Pathol Minneapolis MN 55455 USA

Nitrofluorenes and C-9-oxidized nitrofluorenes are widespread environmental genotoxins which may be relevant for breast cancer on the basis of their carcinogenicities, particularly of 2,7-dinitrofluorene (2,7-diNF), for the rat mammary gland. Since their metabolism to active carcinogens may involve nitroreduction, this study examined the reduction of 2-nitrofluorene (2-NF) and 2,7-diNF and their 9-oxo- and 9-hydroxy (OH) derivatives by the rat mammary gland. Cytosolic fractions catalyze NADH- and NADPH-dependent reductions of the 2-nitro and 9-oxo to the respective 2-amino and 9-OH compounds at rates 4- and greater than or equal to 10-fold greater than those with microsomes. Rates of amine formation catalyzed by cytosol from 2,7-diNF are greater than the rate from 2-NF and increase for C-9-oxidized derivatives: 9-oxo-2-NF > 9-OH-2-NF > 2-NF and 9-OH-2,7-diNF much greater than 9-oxo-2,7-diNF > 2,7-diNF. Nitroreduction is inhibited by O-2 or allopurinol (20 mu M), dicoumarol (100 mu M), and rutin (50 mu M). 9-Oxoreduction is inhibited by rutin, dicoumarol, and indomethacin (100 mu M), but not by O-2 or allopurinol. Pyrazole or menadione does not inhibit nitro or 9-oxoreduction. Xanthine, hypoxanthine, 2-hydroxypyrimidine, and N'-methylnicotinamide support cytosol-catalyzed nitro, but not 9-oxo, reduction. The data suggest that the nitroreduction is catalyzed largely by a xanthine oxidase and partially by a diaphorase and 9-oxoreduction by a carbonyl reductase. The extents of the nitro and carbonyl reductions of the nitrofluorenes may determine their reactivities with DNA, and thus genotoxicities for the mammary gland.

关键词：空气污染物/代谢空气污染物/药理学别嘌呤醇/药理学乳房/药物作用乳房/代谢胞质溶胶/药物作用胞质溶胶/代谢双香豆素/药理学芴类/代谢芴类/药理学次黄嘌呤/药理学吲哚美辛/药理学微粒体/药物作用微粒体/代谢烟酰胺/类似物和衍生物烟酰胺/药理学氧化还原氧/药理学吡唑类/药理学嘧啶类/药理学大鼠 Sprague-Dawley 芦丁/药理学维生素K/药理学黄嘌呤/药理学动物女(雌)性大鼠

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A colorimetric assay for rapid screening of antimicrobial peptides

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NATURE BIOTECHNOLOGY 2000年第2期18卷 225-227页

作者： Kolusheva, S Boyer, L Jelinek, R Ben Gurion Univ Negev Dept Chem IL-84105 Beer Sheva Israel

The increased resistance of various bacteria toward available antibiotic drugs has initiated intensive research efforts into identifying new sources of antimicrobial substances. Short antibiotic peptides (10–30 residues) are prevalent in nature as part of the intrinsic defense mechanisms of most organisms and have been proposed as a blueprint for the design of novel antimicrobial agents^1. Antimicrobial peptides are generally believed to kill bacteria through membrane permeabilization and extensive pore-formation^1. Assays providing rapid and easy evaluation of interactions between antimicrobial membrane peptides and lipid bilayers could significantly improve screening for substances with effective antibacterial properties, as well as contribute to the elucidation of structural and functional properties of antimicrobial peptides. Here we describe a colorimetric sensor in which particles composed of phospholipids and polymerized polydiacetylene (PDA) lipids were shown to exhibit striking color changes upon interactions with antimicrobial membrane peptides. The color changes in the system occur because of the structural perturbation of the lipids following their interactions with antimicrobial peptides. The assay was also sensitive to the antibacterial properties of structurally and functionally related peptide analogs.

关键词：乙炔/类似物和衍生物阿拉霉素/类似物和衍生物阿拉霉素/药理学抗菌药/药理学比色法/方法蜂毒肽/类似物和衍生物蜂毒肽/药理学微生物敏感性试验/方法微粒体/药物作用寡肽类/药理学肽类/药理学通透性磷脂类聚乙炔类聚合物换能器

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