不同激发波长下ZnPcSP的光敏化能力和抗癌活性

研究了激发光的波长对金属酞菁配合物ZnPcSP光敏化产生1O2的能力和光动力抗癌作用的影响．结果表明，激发波长对ZnPcSP配合物光敏化产生1O2的能力和光动力抗癌作用的影响显示了同样的规律性，波长为670um的光具有较佳的激发效率．研究结果同时说明ZnPcSP在光动力治癌中的主要光敏反应机制可能是产生1O2的Ⅱ型反应机制．     

八烷氧基萘酞菁锌的激发三重态性质及光动力抗癌活性

采用激光闪光光解技术测定了系列八烷氧基萘酞菁锌配合物ZnNc(OR)8(R=C4H9,C8H17,C12H25)激发三重态的寿命,研究了该系列化合物光敏化产生单重态氧的能力和对HL60癌细胞的光动力活性,并探讨了它们作为光敏剂在肿瘤光动力治疗中的光敏反应机制。     

八烷氧基萘酞菁锌的激发三重态性质及光动力抗癌活性

采用激光闪光光解技术测定了系列八烷氧基萘酞菁锌配合物ZnNc(OR)8(R=C4H9,C8H17,C12H25)激发三重态的寿命,研究了该系列化合物光敏化产生单重态氧的能力和对HL60癌细胞的光动力活性,并探讨了它们作为光敏剂在肿瘤光动力治疗中的光敏反应机制。     

聚醋酸乙烯酯与铜（Ⅱ）离子的配位反应及其催化作用

以ＥＳＲ、ＵＶ和ＩＲ表征Ｃｕ（２＋）离子与ＰＶＡＣ的配位反应。根据ＣＵＣｌ２·２Ｈ２Ｏ乙醇溶液与ＰＶＡｃ－ＣｕＣｌ２·２Ｈ２Ｏ乙醇溶液的电导率差值随Ｃｕ（２＋）离子摩尔浓度变化的明显转析点得知，１个Ｃｕ（２＋）离子大约能与ＰＶＡｃ４个链节单元配位。证实ＭＭＡ在Ｃｕ（Ⅱ）－ＰＶＡｃ配合物／Ｎａ２ＳＯ３体系的聚合体是无规ＰＭＭＡ，得率为７０％。讨论了ＭＭＡ在Ｃｕ（Ⅱ）－ＰＶＡｃ配合物／Ｎａ２ＳＯ３体系络合催化引发下的游离基反应历程。     

吡啶—2,6—二甲醇配合物[Sc＊HDPA）（DPA）（H2O）2].5H2O的合成及其晶体结构

在水溶液 中合成了吡啶－２，６－二甲酸钪配合物的晶体，元素分析结果表明，可用Ｓｃ（ＨＤＰＡ）（ＤＰＡ）．７Ｈ２Ｏ表示。用Ｘ射线衍射方法测定了配合物的单晶结构，其结构式为［Ｓｃ（ＨＤＰＡ）（ＤＰＡ）（Ｈ２Ｏ２）］５Ｈ２Ｏ。晶体属正交晶系，空间群为Ｐｎ２ｌａ。     

铱(Ⅲ)配合物乏氧肿瘤光动力治疗

光动力治疗因其无创、可控和不易产生耐药性等显著优点,成为一种新型的肿瘤靶向治疗模式。光敏化过程涉及光敏剂对氧分子的光激活反应,然而实体肿瘤的乏氧环境严重限制了传统有机光敏剂的疗效。金属铱配合物具有良好的光物理和光化学性质,是理想的新一代光敏剂,近些年,铱光敏剂被发现可以应用于乏氧肿瘤的光动力治疗。本文总结了近些年金属铱配合物应用于乏氧肿瘤光动力治疗的研究;同时介绍了基于铱配合物的乏氧纳米复合体系的构建和乏氧肿瘤的光动力治疗研究,为开发新型高效的乏氧肿瘤治疗光敏剂及其载体提供参考。     

铱(Ⅲ)配合物乏氧肿瘤光动力治疗

光动力治疗因其无创、可控和不易产生耐药性等显著优点,成为一种新型的肿瘤靶向治疗模式。光敏化过程涉及光敏剂对氧分子的光激活反应,然而实体肿瘤的乏氧环境严重限制了传统有机光敏剂的疗效。金属铱配合物具有良好的光物理和光化学性质,是理想的新一代光敏剂,近些年,铱光敏剂被发现可以应用于乏氧肿瘤的光动力治疗。本文总结了近些年金属铱配合物应用于乏氧肿瘤光动力治疗的研究;同时介绍了基于铱配合物的乏氧纳米复合体系的构建和乏氧肿瘤的光动力治疗研究,为开发新型高效的乏氧肿瘤治疗光敏剂及其载体提供参考。     

La,Nd,Sm,Td与HDBM配合物的固相反应合成与表征

研究了ＨＤＢＭ与Ｌａ，Ｎｄ，Ｓｍ，Ｔｂ等希土离子的固相配位反应，ＲＥＡｃ３．ｘＨ２Ｏ与ＨＤＢＭ进行固相配位反应制备ＲＥ（ＤＢＭ）３配合物，经元素分析，红外，Ｘ衍射和光声光谱检测进行表征。     

酞菁配合物的结构与其光动力抗癌活性

光动力治疗是一种正在发展中的治疗癌症的新方法.主要是利用抗癌光敏剂可优先在 肿瘤组织中富集的特性和随后在适当波长的光照下所引发的光敏化反应来杀死癌肿瘤.自198 5年以来,酞菁配合物作为抗癌光敏剂的研究越来越引人注目. 此文在总结51篇参考文献的 基础上,提出了酞菁配合物的结构与其光动力抗癌活性的某些相关性,着重讨论了中心离子 、环取代基、轴向配体对光动力活性和相关物化性质的影响.得出的一个主要的结论是两亲 性酞菁是极具潜力的光敏剂.     

CS_2在Cu－S键中插入产物（Ph_3P）_2Cu（S_2CSR）与溶剂反应的

ＣＳ_２在Ｃｕ－Ｓ键中插入产物（Ｐｈ_３Ｐ）_２Ｃｕ（Ｓ_２ＣＳＰｈ）与ＣＨ_２Ｃｌ_２－Ｃ_２Ｈ_５ＯＨ混合溶剂反应，获得单核铜配合物（Ｐｈ_３Ｐ）_２Ｃｕ（Ｓ_２ＣＯＯＣ_２Ｈ_５）和双核铜配合物（Ｐｈ_３Ｐ）_３Ｃｕ_２Ｃｌ_２等化合物晶体，用Ｘ－射线单晶衍射法测定前者的晶体结构。晶体的化学式为Ｃ_（３９）Ｈ_（３５）ＣｕＯＰ_２Ｓ_２，分子量为７０９．３，空间群Ｐ２１／ｎ，ａ＝９．３２９（６），ｂ＝１８．６６４（１１），ｃ＝２０，３４１（１３），β＝９５．５９（５）°，Ｖ＝３５２５（４）~３，Ｄ_ｃ＝１．３３７ｇ／ｃｍ~３，Ｚ＝４，Ｆ（０００）＝１４９２，μ＝０．８５２ｍｍ~（－１），Ｒ＝０．０４５。     

抗癌光敏剂ZnPcSP在溶液中的存在状态及其对活性的影响

研究了两亲性抗癌光敏剂磺基邻苯二甲酰亚胺甲基酞菁锌(ZnPcSP)单体与聚集体的可见吸收光谱特征以及溶剂组成对其聚集平衡的影响,得到了ZnPcSP在一系列溶剂中的聚集平衡常数.进而研究了存在状态对ZnPcSP的S₁₈₀肿瘤抑瘤率的影响.ZnPcSP在生理盐水中主要以三聚体形式存在,而在CEL溶液中,则主要以单体形式存在,后者对S180的抑瘤率是前者的8倍     

13-钒镍(锰)杂多酸稀土盐的合成及其镨盐抗肿瘤活性的研究 Ⅰ.

本文以离子交换-复分解法合成了未见文献报道的13-钒镍(锰)杂多酸的稀土盐。通式为Ln2H[MV13O38].nH2O[Ln=La, Ce, Pr, Nd, Sm, Eu; M=Ni, Mn]。经元素分析、红外光谱、电子顺磁共振、磁化率及^5^1V NMR核磁共振谱对其结构进行了表征。微量细胞培养四氮唑(MTT)法实验表明: 13-钒镍(锰)杂多阴离子的镨盐对多种人癌细胞具有较强的杀伤作用, 显示出较强的体外抗肿瘤活性。     

Self-sensitized photodegradation of membrane-bound protoporphyrin mediated by chain lipid peroxidation: inhibition by nitric oxide with sustained singlet oxygen damage

In the presence of exciting light, iron and reductants, the singlet oxygen (1O2)-generating sensitizer protoporphyrin IX (PpIX) induces free radical lipid peroxidation in membranes, but gradually degrades in the process. We postulated that NO, acting as a chain-breaking antioxidant, would protect PpIX against degradation and consequently prolong its ability to produce 1O2. This idea was tested by irradiating PpIX-containing liposomes (LUVs) in the presence of iron and ascorbate, and monitoring the cholesterol hydroperoxides 5alpha-OOH and 7alpha/beta-OOH as respective 1O2 and free radical reporters. 5alpha-OOH accumulation, initially linear with light fluence, slowed progressively after prolonged irradiation, whereas 7alpha/beta-OOH accumulation only accelerated after an initial lag. The active, but not spent, NO donor spermine NONOate (0.4 mM) virtually abolished 7alpha/beta-OOH buildup as well as 5alpha-OOH slowdown. Increasing membrane phospholipid unsaturation hastened the onset of rapid chain peroxidation and 5alpha-OOH slowdown. Accompanying the 5alpha-OOH effect was a steady decrease in 1O2 quantum yield and PpIX fluorescence at 632 nm, both of which were inhibited by NO. An NO-inhibitable decay of PpIX fluorescence was also observed during dark incubation of 5alpha-OOH-bearing LUVs with iron and ascorbate, confirming a link between chain peroxidation and PpIX loss. By protecting PpIX in irradiated membranes, NO might select for and prolong purely 1O2-mediated damage. Supporting this was our observation that 1O2-mediated photoinactivation of a nonmembrane target, lactate dehydrogenase, slowed concurrently with 5alpha-OOH accumulation and that spermine NONOate prevented this. Thus, NO not only protected membrane lipids against PpIX-sensitized free radical damage, but PpIX itself, thereby extending its 1O2-generating lifetime. Consistent findings were obtained using porphyrin-sensitized COH-BR1 cells. These previously unrecognized effects of NO could have important bearing on 5-aminolevulinate-based photodynamic therapy in which PpIX is metabolically deposited in tumor cells.     

Biological activities of phthalocyanines--III. Photoinactivation of V-79 Chinese hamster cells by tetrasulfophthalocyanines

Abstract— Tetrasulfophthalocyanine and a series of its metal chelates were tested for their ability to photoinactivate V-79 Chinese hamster cells. Incubation of cells for 1 h with tetrasulfophthalocyanine at 5 μM effectively sensitized cells towards red light. At the 1% survival level, the dye was 4 x more efficient than hematoporphyrin, efficiency being defined in terms of drug concentration in the medium and incident light fluence rather than on the basis of quanta absorbed. Chelation of the dye with metal ions resulted in most cases in a greatly diminished photosensitizing effect, except for cerium. The cerium complex was about 5 x more effective for cell killing than the metal free tetrasulfophthalocyanine and 20 x more efficient as compared to hematoporphyrin. Hypoxic conditions resulted in total loss of photoactivity indicating the involvement of oxygen in the action mechanism. The inactivation by near-UV light by these drugs was also investigated. The potential of sulfonated phthalocyanines as novel photosensitizers for photodynamic cancer therapy is discussed.     

Synergistic enhanced photocatalytic and photothermal activity of Au@TiO2 nanopellets against human epithelial carcinoma cells

The photocatalytic and plasmonic photothermal cancer cell-killing activity of the metallic Au-capped TiO(2) (Au@TiO(2)) composite colloidal nanopellets has been investigated on HeLa cells under UV-visible (350-600 nm) light irradiation. The Au@TiO(2) composite nanopellets with the uniform Au-capped TiO(2) structure were successfully synthesized by simple reduction of HAuCl(4) on the surface of TiO(2) nanoparticles. The morphological structure and surface properties of Au@TiO(2) were characterized by using UV-visible absorption spectroscopy, TEM, SEM, XPS, EDX and XRD analyses. The formation of hydroxyl radicals (˙OH) was confirmed by photoluminescence (PL) spectra. The photocatalytic and photothermal cell-killing activity of the Au@TiO(2) nanopellets was found to vary with the molar ratio of Au to TiO(2). The direct involvement of the metal particles in mediating the electron transfer from the photoexcited TiO(2) under the band gap excitation is considered to carry out the efficient photocatalytic reaction on the cells. The plasmonic absorption spectra of Au@TiO(2) suspensions were also measured for the evaluation of photothermal cell killing. The charge separation, the interfacial charge-transfer and photothermal activity promoted the photocatalytic-photothermal cancer-cell killing more than TiO(2) alone. The cytotoxic effect of Au@TiO(2) nanopellets with low concentration of gold (TiO(2) : Au molar ratio > 1 : 1) was found to be 100%, whereas that of the commercial TiO(2) (P25) was ca. 50%. The comparative study of the cell viability using Au alone and TiO(2) alone revealed that the synergistic effect of photocatalytic hydroxyl radical formation and Au-plasmonic photothermal heat generation plays a vital role in the cancer cell killing. A plausible mechanism was also proposed for photocatalytic cancer cell killing based on the obtained results.     

pH-responsive NIR enhanced drug release from gold nanocages possesses high potency against cancer cells

We report a smart therapeutic nanoplatform based on Fe(3)O(4)@CaP capped gold nanocages, which integrates magnetic targeting, photothermal therapy and chemotherapy for killing cancer cells. Combining photothermal- and chemo-therapy results in a synergistic effect in cancer treatment.     

PHOTOSENSITIZED INACTIVATION OF CHINESE HAMSTER CELLS BY PHTHALOCYANINES

Chloroaluminum phthalocyanine was found to sensitize cultured Chinese hamster cells upon exposure to white fluorescent light. Elimination of wavelengths below 370 nm did not reduce the effect significantly, indicating that the effective wavelengths were those absorbed by the Q band (600–700 nm) of phthalocyanine. The magnitude of the photosensitizing effect increased with the dye concentration and the time of its contact with the cells prior to light exposure. Although photosensitization was drastically reduced in the absence of oxygen, the lack of effect of glycerol and D₂0 during exposure suggests that neither hydroxyl radicals nor ¹O₂ are responsible for the cytotoxic response. The efficiency of the photosensitized induced cell killing did not vary with the position of the cells in the cell cycle, in contrast to exposure to X-rays. The improved spectral properties, the reported low toxicity and the selective retention by neoplasms, make phthalocyanines promising candidates for use in photodynamic therapy of cancer.     

Multifunctional Core–Shell Upconverting Nanoparticles for Imaging and Photodynamic Therapy of Liver Cancer Cells

Lanthanide‐doped upconversion nanoparticles (UCNPs) have attracted considerable attention for their application in biomedicine. Here, silica‐coated NaGdF₄:Yb,Er/NaGdF₄ nanoparticles with a tetrasubstituted carboxy aluminum phthalocyanine (AlC₄Pc) photosensitizer covalently incorporated inside the silica shells were prepared and applied in the photodynamic therapy (PDT) and magnetic resonance imaging (MRI) of cancer cells. These UCNP@SiO₂(AlC₄Pc) nanoparticles were uniform in size, stable against photosensitizer leaching, and highly efficient in photogenerating cytotoxic singlet oxygen under near‐infrared (NIR) light. In vitro studies indicated that these nanoparticles could effectively kill cancer cells upon NIR irradiation. Moreover, the nanoparticles also demonstrated good MR contrast, both in aqueous solution and inside cells. This is the first time that NaGdF₄:Yb,Er/NaGdF₄ upconversion‐nanocrystal‐based multifunctional nanomaterials have been synthesized and applied in PDT. Our results show that these multifunctional nanoparticles are very promising for applications in versatile imaging diagnosis and as a therapy tool in biomedical engineering.     

结合电生孔技术的抗体-纳米TiO2靶向光敏杀癌细胞

报道了用免疫、电生孔和纳米TiO₂光催化组合技术进行杀伤结肠癌LoVo细胞的研究. 先把结合LoVo细胞表面CEA抗原的单克隆抗CEA抗体吸附在纳米TiO₂微粒表面, 抗体-纳米TiO₂复合微粒就会自动吸附到LoVo细胞的表面, 然后用电脉冲法使LoVo癌细胞的细胞膜上产生小孔, 促使纳米TiO₂微粒进入癌细胞内部. 最后在紫外光照射下使TiO₂纳米粒子在癌细胞内部发生光催化氧化作用, 杀伤癌细胞. 结果表明, 这种组合技术具有很高的杀癌细胞能力. 在仅含3.12 μg/mL抗体-纳米TiO₂的细胞培养液内和强度为4 mW/cm²的紫外光照射下, 可在30 min内将所有LoVo癌细胞杀死. 这种技术对LoVo癌细胞的杀伤力远高于对不表达CEA抗原的人正常TE353.sk细胞的杀伤力, 显示了组合技术杀癌细胞的高选择性. 因此, 这种组合技术有望成为治疗癌症的新方法, 值得进一步探索.     

基于NaYF_4∶Yb~(3+),Er~(3+)上转换发光纳米晶的复合微球组装及其光动力活性

采用微乳液法,以NaYF4∶Yb3+,Er3+纳米晶为发光基元,肽菁锌(Zn Pc)光敏分子与十八碳烯-马来酸酐共聚物(PMAO)为功能分子,一步组装获得了NaYF4-Zn Pc-PMAO复合微球,此微球同时具备成像与光动力活性功能,NaYF4可作为低生物背景的荧光成像剂,同时其上转换发光可以敏化Zn Pc用于光动力活性研究,PMAO分子经过简单的水解反应即可实现表面羧基功能化。TEM,Zeta电位与PL测试证实了微球的结构与性能。利用荧光共聚焦成像技术实现了对Hela细胞的发光成像;进一步通过单线态氧监测及980 nm光照下的MTT法细胞活性测试表明微球具有光动力活性功能。