formazans has been researched along with Neoplasms* in 12 studies
12 other study(ies) available for formazans and Neoplasms
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Self-assembled organic nanomedicine enables ultrastable photo-to-heat converting theranostics in the second near-infrared biowindow.
Development of organic theranostic agents that are active in the second near-infrared (NIR-II, 1000-1700 nm) biowindow is of vital significance for treating deep-seated tumors. However, studies on organic NIR-II absorbing agents for photo-to-heat energy-converting theranostics are still rare simply because of tedious synthetic routes to construct extended π systems in the NIR-II region. Herein, we design a convenient strategy to engineer highly stable organic NIR-II absorbing theranostic nanoparticles (Nano-BFF) for effective phototheranostic applications via co-assembling first NIR (NIR-I, 650-1000 nm) absorbing boron difluoride formazanate (BFF) dye with a biocompatible polymer, endowing the Nano-BFF with remarkable theranostic performance in the NIR-II region. In vitro and in vivo investigations validate that Nano-BFF can serve as an efficient theranostic agent to achieve photoacoustic imaging guided deep-tissue photonic hyperthermia in the NIR-II biowindow, achieving dramatic inhibition toward orthotopic hepatocellular carcinoma. This work thus provides an insight into the exploration of versatile organic NIR-II absorbing nanoparticles toward future practical applications. Topics: Animals; Cell Line, Tumor; Formazans; Hot Temperature; Infrared Rays; Light; Mice, Inbred C57BL; Neoplasms; Organic Chemicals; Photoacoustic Techniques; Photothermal Therapy; Theranostic Nanomedicine | 2021 |
Cisplatin-loaded gelatin-poly(acrylic acid) nanoparticles: synthesis, antitumor efficiency in vivo and penetration in tumors.
Cisplatin (CDDP)-loaded gelatin-poly(acrylic acid) (GEL-PAA) nanoparticles were successfully prepared by polymerizing acrylic acid in the presence of gelatin in aqueous solution followed by incorporating CDDP into the formed GEL-PAA nanoparticles through polymer-metal complex formation of CDDP with carboxylic groups in the nanoparticles. The obtained nanoparticles had a spherical shape, with a mean size of about 100 nm, and high drug payload as well as stability. It is found that CDDP can be released from the nanoparticles in a sustained manner with a small initial burst release. In vitro cytotoxicity revealed that CDDP-loaded nanoparticles had similar cytotoxicity to free CDDP after 48 h co-incubation with human colorectal cancer cell line LoVo. In vivo antitumor activity indicated that the nanoparticle formulation was superior in anticancer effect to free CDDP on murine hepatic H22 tumor-bearing mice model through intraperitoneal (i.p.) administration and displayed a dose-dependent antitumor efficacy. Further, the penetration examination of the nanoparticles through tumor tissue revealed that the CDDP-loaded GEL-PAA nanoparticles could only affect the cells near the tumor vasculature after they entered into the tumor tissue. Topics: Acrylates; Animals; Antineoplastic Agents; Cisplatin; Dose-Response Relationship, Drug; Drug Carriers; Drug Compounding; Drug Delivery Systems; Drug Evaluation, Preclinical; Drug Stability; Formazans; Gelatin; Humans; Male; Mice; Mice, Inbred ICR; Nanoparticles; Neoplasms; Tetrazolium Salts; Xenograft Model Antitumor Assays | 2011 |
Docetaxel-loaded-lipid-based-nanosuspensions (DTX-LNS): preparation, pharmacokinetics, tissue distribution and antitumor activity.
The purpose of the study was to design lipid-based-nanosuspensions (LNS) for Docetaxel (DTX) without Tween 80 for clinical intravenous administration (i.v.). DTX-LNS were prepared by high pressure homogenization method, and then lyophilization was carried out to improve the stability. The physical-chemical properties in terms of particle size, size distribution, zeta potential and morphology were evaluated, respectively. The in vitro cytotoxic activity was assessed by MTT against SKOV-3 and malignant melanoma B16 cells. The in vivo pharmacokinetics, tissue distribution as well as antitumor efficacy were investigated in B16 melanoma-bearing Kunming mice. The particle size and zeta potential of DTX-LNS were (200.0 ± 3.42)nm and (-11.15 ± 0.99)mV, respectively. Compared with Duopafei, it was shown that DTX-LNS exhibited higher antitumor efficacy by reducing tumor volume (P<0.05) and increasing survival rate in B16 melanoma-bearing mice and strongly reduced the anticancer drug toxicity. The results of biodistribution studies clearly indicated the superiority of DTX-LNS to Duopafei in increasing the accumulation of DTX within tumor and the organs rich in macrophages (liver, lungs and spleen), while, the drug concentration in heart and kidney decreased. Together these results suggested that DTX-LNS could effectively inhibit tumor growth, reduce toxicity during the therapeutic procedure and hold the potential to be an appropriate choice for the clinical administration of DTX. Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Docetaxel; Drug Carriers; Drug Compounding; Drug Delivery Systems; Excipients; Female; Formazans; Humans; Lecithins; Lipids; Melanoma; Mice; Nanoparticles; Neoplasms; Ovarian Neoplasms; Particle Size; Suspensions; Taxoids; Tetrazolium Salts; Tissue Distribution | 2011 |
Myrseguinosides A-E, five new glycosides from the fruits of Myrsine seguinii.
Chemical investigation of the 1-BuOH soluble fraction of the dried fruits of Myrsine seguinii (Myrsinaceae) led to the isolation of five new glycosides, named myrseguinosides A-E (1-5), together with eight known compounds (6-13). The absolute structures of the new glycosides were elucidated by spectroscopic and chemical analyses to be a monoterpene glucoside (1), two flavonol glycosides (2, 3), and two oleanane-type triterpene saponins (4, 5). Myrseguinosides B (2), D (4), and E (5) exhibited 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical-scavenging activity and growth inhibitory activity toward human cancer cells, respectively. Topics: Anticarcinogenic Agents; Biphenyl Compounds; Cell Line, Tumor; Drug Screening Assays, Antitumor; Formazans; Fruit; Glycosides; HL-60 Cells; Humans; Inhibitory Concentration 50; Molecular Structure; Neoplasms; Phytotherapy; Picrates; Plant Extracts; Primulaceae; Structure-Activity Relationship; Tetrazolium Salts | 2011 |
Constituents of Corydalis heterocarpa and their anti-proliferative effects on human cancer cells.
Two new coumarins, 1 and 2, along with four known coumarins (3-6) have been isolated from Corydalis heterocarpa. On the basis of spectroscopic and chemical methods, compounds 1 and 2 were elucidated as (2'S,7'S)-O-2-methylbutanoyl-columbianetin and (2'S)-columbianetin-3'-sulfate, respectively. The anti-proliferative activity against human cancer cells of compounds 1-6 isolated from C. heterocarpa was evaluated using a MTT assay and by mRNA expression of several factors related to apoptosis. Among them, compound 2 exerted the more potent anti-proliferative activity compared with the other compounds treated. The potent inhibitory effect of compound 2 was produced by induction of apoptosis through activating Bax, p53 and p21 expressions. Topics: Adenocarcinoma; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Survival; Corydalis; Coumarins; Drug Screening Assays, Antitumor; Female; Formazans; Humans; Neoplasms; Plant Extracts; Tetrazolium Salts | 2010 |
Screen anticancer drug in vitro using resonance light scattering technique.
An in vitro screening model using resonance light scattering (RLS) technique with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) reagent as the reactive probe to target cancer cell was firstly developed. In this model, MTT was reduced by viable cancer cells to produce a purple formazan. Cell viability was proportional to the number of formazan induced strong light scattering signal. The inhibition rate of anticancer drug was found to vary inversely with the H(22)-MTT system RLS intensity. So it was intuitive to see the sequence of the tumor suppressive activity of six anticancer drugs without data processing by RLS/MTT screening spectra. Compared with the traditional MTT method, this method has high sensitivity, low detection limit and quite intuitive screening results which were identical to those obtained from the MTT colorimetric assay. Topics: Animals; Antineoplastic Agents; Carcinoma, Hepatocellular; Colorimetry; Drug Screening Assays, Antitumor; Formazans; Humans; Inhibitory Concentration 50; Light; Mice; Neoplasms; Scattering, Radiation; Sensitivity and Specificity; Tetrazolium Salts; Thiazoles; Time Factors | 2009 |
Photooxidative action in cancer and normal cells induced by the use of photofrin in photodynamic therapy.
Photofrin-mediated PDT was applied to malignant (A549 and MCF-7) and normal (HUV-EC-C) cells. The cells were incubated for different lengths of time after PDT. The cell responses to the therapy were examined by changes in SOD activity, phototoxicity, and mode of the cell death. PDT induced dynamic changes in SOD activity. Initially, an increase in SOD activity was observed, and after 6 hours of culture it decreased to the control level. Results obtained from MTT and the comet assay indicate that PDT caused immediate cell death via apoptosis in the A549, MCF-7, and HUV-EC-C cell lines. Our studies confirm that SOD is involved in the response of both cancer and normal cells to PDT. Topics: Aged; Cell Line, Tumor; Comet Assay; Dihematoporphyrin Ether; Female; Formazans; Humans; Light; Male; Middle Aged; Neoplasms; Oxidation-Reduction; Photochemotherapy; Photosensitizing Agents; Superoxide Dismutase; Tetrazolium Salts | 2008 |
Naturally occurring resistance of bone marrow mononuclear and metastatic cancer cells to anticancer agents.
Numerous cancer patients fail standard chemotherapy or develop resistance to chemotherapy during the course of treatment. The purpose of this study is to elucidate the overall response of cells obtained from cancer patients and from normal individuals to chemotherapeutic agents. We analysed the chemosensitivity of cancer cells derived from bone marrow and from pleural effusions or ascites fluids from patients with different cancers. Chemosensitivity to doxorubicin, cisplatin and paclitaxel was determined using the MTT assay. We also determined the response of bone marrow mononuclear (BMMN) cells. There was a wide range of responses to chemotherapy drugs in samples from different individuals. This was observed in cells derived from bone marrow and from ascites or pleural fluids. Large variations were also observed among morphologically normal BMMN cells and metastatic cancer cells from chemo-naïve patients. Cancer cells can easily be collected from ascites or pleural fluids and reliably assayed for chemosensitivity. We describe here that inherent chemoresistance may be a reason for the lack of response to chemotherapy in some patients. We discuss the potential of using the determination of natural resistance to dictate the drugs to be employed for treatment. Topics: Antineoplastic Agents; Ascitic Fluid; Bone Marrow Cells; Cell Survival; Cisplatin; Dose-Response Relationship, Drug; Doxorubicin; Drug Resistance, Neoplasm; Female; Formazans; Humans; Inhibitory Concentration 50; Male; Neoplasm Metastasis; Neoplasms; Neoplastic Stem Cells; Paclitaxel; Pleural Effusion, Malignant; Tetrazolium Salts | 2006 |
Effect of NQO1 induction on the antitumor activity of RH1 in human tumors in vitro and in vivo.
NQO1 is a reductive enzyme that is important for the activation of many bioreductive agents and is a target for an enzyme-directed approach to cancer therapy. It can be selectively induced in many tumor types by a number of compounds including dimethyl fumarate and sulforaphane. Mitomycin C is a bioreductive agent that is used clinically for treatment of solid tumors. RH1 (2,5-diaziridinyl-3-(hydroxymethyl)- 6-methyl-1,4-benzoquinone) is a new bioreductive agent currently in clinical trials. We have shown previously that induction of NQO1 can enhance the antitumor activity of mitomycin C in tumor cells in vitro and in vivo. As RH1 is activated selectively by NQO1 while mitomycin C is activated by many reductive enzymes, we investigated whether induction of NQO1 would produce a greater enhancement of the antitumor activity of RH1 compared with mitomycin C. HCT116 human colon cancer cells and T47D human breast cancer cells were incubated with or without dimethyl fumarate or sulforaphane followed by mitomycin C or RH1 treatment, and cytotoxic activity was measured by a clonogenic (HCT116) or MTT assay (T47D). Dimethyl fumarate and sulforaphane treatment increased NQO1 activity by 1.4- to 2.8-fold and resulted in a significant enhancement of the antitumor activity of mitomycin C, but not of RH1. This appeared to be due to the presence of a sufficient constitutive level of NQO1 activity in the tumor cells to fully activate the RH1. Mice were implanted with HL60 human promyelocytic leukemia cells, which have low levels of NQO1 activity. The mice were fed control or dimethyl fumarate-containing diet and were treated with RH1. NQO1 activity in the tumors increased but RH1 produced no antitumor activity in mice fed control or dimethyl fumarate diet. This is consistent with a narrow window of NQO1 activity between no RH1 activation and maximum RH1 activation. This study suggests that selective induction of NQO1 in tumor cells is not likely to be an effective strategy for enhancing the antitumor activity of RH1. In addition, we found that RH1 treatment produced significant leukopenia in mice that may be of concern in the clinic. These results suggest that the ease of reduction of RH1 by NQO1 makes it a poor candidate for an enzyme-directed approach to cancer therapy. Topics: Animals; Antineoplastic Agents; Aziridines; Benzoquinones; Cell Line, Tumor; Cell Survival; Dose-Response Relationship, Drug; Enzyme Induction; Female; Formazans; Leukopenia; Mice; Mice, Inbred Strains; Mice, Nude; Mitomycin; NAD(P)H Dehydrogenase (Quinone); NADPH Dehydrogenase; Neoplasms; Tetrazolium Salts; Toxicity Tests; Xenograft Model Antitumor Assays | 2005 |
Maillard reaction products modulating the growth of human tumor cells in vitro.
We investigated the effect of a series of Maillard reaction products formed from carbohydrates under household heating conditions on the growth of human tumor cells in vitro. 4-Hydroxy-5-methyl-3-(2H)-furanone (1) was found to potently enhance the proliferation of human tumor cells. In contrast, the Maillard-type chromophores 2-(2-furyl)methylidene-4-hydroxy-5-methyl-2H-furan-3-one (2), 4-(2-furyl)-7-[(2-furyl)methylidene]-2-hydroxy-2H,7H,8aH-pyrano[2,3-b]- pyran-3-one (6), and 3-hydroxy-4[(E)-(2-furyl)methylidene]methyl-3-cyclopentene-1,2 dione (13) inhibited the growth of human tumor cells in vitro in the low micromolar range. GXF251L cells (gastric carcinoma), synchronized by serum deprivation, were retained in the G1-phase of the cell cycle after treatment with 2, 6, or 13 for 24 h. Concomitantly, a distinct sub-G1 peak was observed, indicative for apoptosis induction. DNA fragmentation was further investigated by ELISA using antibodies raised against histones and DNA. 2 induced a significant increase of fragmented DNA at concentrations > or = 30 microM. After treatment with compound 6, DNA fragmentation was observed at a higher concentration range (> or = 50 microM), whereas incubation with 13 resulted in a marked DNA fragmentation already at 20 microM. On the protein level, the activation of caspase 3, as an early marker for apoptosis induction, was determined. The results were almost identical to those obtained in the DNA fragmentation ELISA. In summary, Maillard reaction products potently modulating the growth of human tumor cells were identified. The Maillard-type chromophores 2, 6, and 13 were found to interfere with the proliferation of gastric carcinoma cells, causing cell cycle arrest and apoptosis induction. Topics: Antineoplastic Agents; Apoptosis; Caspase 3; Caspases; Cell Cycle; Cyclopentanes; DNA Fragmentation; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; Formazans; Furans; Humans; Maillard Reaction; Neoplasms; Tetrazolium Salts; Tumor Cells, Cultured | 2003 |
Differential sensitivity of various pediatric cancers and squamous cell carcinomas to lovastatin-induced apoptosis: therapeutic implications.
3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase is the rate-limiting enzyme of the mevalonate pathway, the diverse array of end products of which are vital for a variety of cellular functions, including cholesterol synthesis and cell cycle progression. We showed previously that this enzyme holds a critical role in regulating tumor cell fate, including cell death, as its expression is down-regulated in response to retinoic acid, a potent anticancer therapeutic. Indeed, direct inhibition of HMG-CoA reductase with lovastatin, a competitive inhibitor of this enzyme, induced a pronounced apoptotic response in neuroblastoma and acute myeloid leukemic cells. We have now extended this work and evaluated a wide variety and large number of tumor-derived cell lines for their sensitivity to lovastatin-induced apoptosis. These cell lines were exposed to a wide range (0-100 microM) of lovastatin for 2 days and assayed for cell viability using the 3,4,5-dimethyl thiazlyl-2,2,5-diphenyltetrazolium bromide assay and the induction of apoptosis by flow cytometric and ultrastructural analyses. Lovastatin induced a pronounced apoptotic response in cells derived from juvenile monomyelocytic leukemia, pediatric solid malignancies (rhabdomyosarcoma and medulloblastoma), and squamous cell carcinoma of the cervix and of the head and neck. Interestingly, the subset of malignancies that are particularly sensitive to lovastatin-induced apoptosis correspond to those tumor subtypes that are sensitive to the biological and antiproliferative effects of retinoids in vitro. The nature of the biologically active form of lovastatin has been challenged recently as the growth-inhibitory effects of this drug were attributed to its prodrug lactone form that does not inhibit HMG-CoA reductase function. In this report, we demonstrate that the apoptotic properties of lovastatin are triggered by the open ring acid form that is a potent inhibitor of HMG-CoA reductase activity. Thus, we have identified a subset of tumors that are sensitive to lovastatin-induced apoptosis and show HMG-CoA reductase as a potential therapeutic target of these cancers. Topics: Adult; Antineoplastic Agents; Apoptosis; Child; Chromatography, High Pressure Liquid; Female; Flow Cytometry; Formazans; Humans; Hydroxymethylglutaryl CoA Reductases; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Lovastatin; Mass Spectrometry; Mevalonic Acid; Microscopy, Electron; Neoplasms; Tetrazolium Salts; Tumor Cells, Cultured | 2001 |
DNA breakage by resveratrol and Cu(II): reaction mechanism and bacteriophage inactivation.
Resveratrol (3,4',5-trihydroxy stilbene) is a phytoalexin and a polyphenolic compound present in human dietary material such as peanuts, mulberries, grapes and red wine. It is widely considered to possess cardiovascular protective properties and has also been shown to be chemopreventive against various stages of chemically induced carcinogenesis. It has recently been shown that resveratrol induces strand breakage in DNA in the presence of copper ions. In this paper, we have shown that resveratrol catalyzes the reduction of Cu(II) to Cu(I), which is accompanied by the formation of 'oxidized product(s)' of resveratrol, which in turn also appear to catalyze the reduction of Cu(II). Strand scission by the resveratrol-Cu(II) system was found to be biologically active as assayed by bacteriophage inactivation. The results are discussed in relation to the putative chemopreventive mechanism of resveratrol. Topics: Animals; Anticarcinogenic Agents; Bacteriophage lambda; Cattle; Copper; DNA; DNA Damage; Dose-Response Relationship, Drug; Endoribonucleases; Formazans; Free Radical Scavengers; Ions; Neoplasms; Phenanthrolines; Reactive Oxygen Species; Resveratrol; Spectrophotometry; Stilbenes; Thymus Gland; Time Factors; Ultraviolet Rays | 2000 |