formazans and Melanoma

formazans has been researched along with Melanoma* in 12 studies

Other Studies

12 other study(ies) available for formazans and Melanoma

ArticleYear
Docetaxel-loaded-lipid-based-nanosuspensions (DTX-LNS): preparation, pharmacokinetics, tissue distribution and antitumor activity.
    International journal of pharmaceutics, 2011, Jul-15, Volume: 413, Issue:1-2

    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
Silymarin selectively protects human renal cells from cisplatin-induced cell death.
    Pharmaceutical biology, 2011, Volume: 49, Issue:10

    Cisplatin-induced nephrotoxicity has been accepted as an important obstacle for efficient cisplatin-based chemotherapy. Silymarin from seeds of milk thistle [Silybum marianum L. (Asteraceae)] has been shown to possess various potential pharmacological properties; however, whether or not this agent selectively protects renal cells from cisplatin-induced cell death with no interfering effect on cancer cells is not clear.. Potential of silymarin in protection of cisplatin-induced renal cell death without compromising effect on anticancer activity of cisplatin was demonstrated in this study.. Cisplatin-induced cell death was evaluated in human proximal tubular HK-2, lung carcinoma H460, and melanoma G361 cells using MTT, Hoechst 33342, and propidium iodide assays.. Cisplatin induced both apoptosis and necrosis in HK-2 cells and caused a decrease in cell viability by ~40% and 60% at the doses of 25 and 100 µM, respectively. Pretreatment with 25-200 µM of silymarin significantly protected against cisplatin-induced cell death in a dose-dependent manner. In contrast, pretreatment of silymarin (25-100 µM) caused no significant change on cisplatin-induced cell death in H460 cells but significantly potentiated cisplatin-induced apoptosis in G361 cells.. These findings reveal the selectivity of silymarin in protection of renal cells from cisplatin-induced cell death and could be beneficial for the development of this considerately safe compound as a renoprotective agent.

    Topics: Acute Kidney Injury; Antineoplastic Agents; Antioxidants; Apoptosis; Benzimidazoles; Cell Death; Cell Survival; Cisplatin; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Formazans; Humans; Kidney; Lung Neoplasms; Melanoma; Propidium; Protective Agents; Silybum marianum; Silymarin; Tetrazolium Salts; Tumor Cells, Cultured

2011
Modulation of antioxidant defense by Alpinia galanga and Curcuma aromatica extracts correlates with their inhibition of UVA-induced melanogenesis.
    Cell biology and toxicology, 2010, Volume: 26, Issue:2

    Ultraviolet A (UVA) irradiation is suggested to contribute to melanogenesis through promoting cellular oxidative stress and impairing antioxidant defenses. An overproduction of melanin can be associated with melanoma skin cancer and hyperpigmentation. Therefore, developing effective antimelanogenic agents is of importance. Alpinia galanga (AG) and Curcuma aromatica (CA) are traditional medicinal plants widely used for skin problems. Hence, this study investigated the antimelanogenic effects of AG and CA extracts (3.8-30 microg/ml) by assessing tyrosinase activity, tyrosinase mRNA levels, and melanin content in human melanoma cells (G361) exposed to UVA. The roles in protecting against melanogenesis were examined by evaluating their inhibitory effects on UVA-induced cellular oxidative stress and modulation of antioxidant defenses including antioxidant enzymes, catalase (CAT) and glutathione peroxidase (GPx), and intracellular glutathione (GSH). In addition, possible active compounds accountable for biological activities of the extracts were identified by thin layer chromatography (TLC)-densitometric analysis. Our study demonstrated that UVA (8 J/cm(2)) induced both tyrosinase activity and mRNA levels and UVA (16 J/cm(2))-mediated melanin production were suppressed by the AG or CA extracts at noncytotoxic concentrations. Both extracts were able to protect against UVA-induced cellular oxidant formation and depletion of CAT and GPx activities and GSH content in a dose-dependent manner. Moreover, TLC-densitometric analysis detected the presence of eugenol and curcuminoids in AG and CA, respectively. This is the first report representing promising findings on AG and CA extract-derived antityrosinase properties correlated with their antioxidant potential. Inhibiting cellular oxidative stress and improving antioxidant defenses might be the mechanisms by which the extracts yield the protective effects on UVA-dependent melanogenesis.

    Topics: Alpinia; Catalase; Cell Line, Tumor; Cell Survival; Curcuma; Drug Screening Assays, Antitumor; Formazans; Gene Expression Regulation, Enzymologic; Glutathione; Glutathione Peroxidase; Humans; L-Lactate Dehydrogenase; Melanins; Melanocytes; Melanoma; Monophenol Monooxygenase; Oxidative Stress; Plant Extracts; Tetrazolium Salts; Ultraviolet Rays

2010
Curcumin induces cell death in human uveal melanoma cells through mitochondrial pathway.
    Current eye research, 2010, Volume: 35, Issue:4

    To study the cytotoxic effects and related signaling pathways of curcumin on human uveal melanoma cells in vitro.. Two human uveal melanoma cell lines (M21 and SP6.5), scleral fibroblasts, and choroidal melanocytes were treated with curcumin. The effects of curcumin on cell viability were assessed by using the MTT (3-[4,5-dimethylthiazol-2-yl]2,5-diphenyltetrazolium bromide) assay. Cytosol cytochrome c levels and the activities of caspase-9 and caspase-3 were measured by using an enzyme-linked immunosorbent assay.. Curcumin induced cell death of cultured human uveal melanoma cells in a dose-dependent manner (10, 30, and 100 microM) and time-dependent manner (3-48 hr), with IC50 at 19.05 microM and 22.39 microM in M21 and SP6.5 cell lines, respectively. Curcumin at lower concentrations (10-30 microM) selectively reduced the cell viability of uveal melanoma cells, without affecting cell viability of fibroblasts and choroidal melanocytes. Curcumin significantly increased the level of cytosol cytochrome c (2-fold greater than the controls after 2 hr treatment), caspase-9 and caspase-3 activities (approximately 4.5- and 6-fold greater than the controls after 2-6 hr treatment, respectively) in a dose-dependent manner.. Curcumin has selectively potent cytotoxic effects on cultured human uveal melanoma cells. This effect is associated with the release of cytochrome c from the mitochondria and the activation of caspase-9 and caspase-3 in uveal melanoma cells after treatment with curcumin.

    Topics: Antineoplastic Agents; Caspase 3; Caspase 9; Cell Death; Cell Survival; Curcumin; Cytochromes c; Cytosol; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; Fibroblasts; Formazans; Humans; Melanocytes; Melanoma; Tetrazolium Salts; Time Factors; Tumor Cells, Cultured; Uveal Neoplasms

2010
Cytotoxic, genotoxic and oxidative stress induced by 1,4-naphthoquinone in B16F1 melanoma tumor cells.
    Toxicology in vitro : an international journal published in association with BIBRA, 2009, Volume: 23, Issue:2

    Quinones have diverse pharmacological properties including antibacterial, antifungal, antiviral, anti-inflammatory, antipyretic and anticancer activity. The cytotoxic potential of 1,4-naphthoquinone (NQ14) was studied against B16F1 melanoma cells grown in vitro. NQ14 treatment resulted in a concentration-dependent cytotoxicity as indicated by MTT assay and lactate dehydrogenase leakage assay. Depletion in cellular glutathione levels after 1h incubation with NQ14 correlated with the corresponding increase in reactive oxygen species generation as determined by 2',7'-dicholorofluorescein diacetate assay suggests the role of oxidative stress in cell death. The frequency of micronucleated binucleate cells increased with increasing doses of NQ14 with a corresponding decrease in the cytokinesis block proliferation index indicating the drug induced genotoxicity and cell division delay. Further, a dose-dependent decrease in the clonogenic cell survival indicated the potential of NQ14 to inhibit cell proliferation contributing to cell death. The cell death after NQ14 treatment may be attributed to apoptosis as seen in DNA ladder pattern along with necrosis as indicated in flow cytometric analysis of Annexin V/PI stained cells. Results of the present study demonstrate the cytotoxic and genotoxic potential of NQ14 by the induction of oxidative stress mediated mechanisms leading to tumor cell kill.

    Topics: Animals; Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Survival; Dose-Response Relationship, Drug; Drug Screening Assays, Antitumor; Formazans; Glutathione; L-Lactate Dehydrogenase; Melanoma; Mice; Micronucleus Tests; Naphthoquinones; Necrosis; Oxidative Stress; Reactive Oxygen Species; Tetrazolium Salts

2009
The protective effect of silibinin against mitomycin C-induced intrinsic apoptosis in human melanoma A375-S2 cells.
    Journal of pharmacological sciences, 2009, Volume: 111, Issue:2

    Silibinin is known for its hepatoprotective, anti-inflammatory, and anti-carcinogenic effects. We found that silibinin exhibited a protective effect against chemotherapeutic reagent mitomycin C-induced cell death in A375-S2 cells in a p53-dependent manner, which contradicted the findings of previous studies investigating the anti-neoplastic activity of silibinin and developing silibinin as a potential anti-neoplastic drug in clinical therapy. Mitomycin C administration triggered a time- and dose-dependent cell death in A375-S2 cells. Apoptotic morphology, DNA fragmentation, and caspase-3 activation demonstrated that the major cause of A375-S2 cell death by mitomycin C was apoptosis. This was associated with a marked increase of p53 level and changes in mitochondria associated proteins. However, preincubation with silibinin prior to mitomycin C treatment substantially suppressed cell apoptosis, attenuated the change of p53 and Bcl-2 expressions, blocked the translocation of Bax to mitochondrial outer membrane, and ameliorated the loss of mitochondrial membrane potential, but mitomycin C stimuli led to few changes in the protein levels of caspase 8, Fas ligand, and Fas-associated death domain protein, indicating that silibinin protected cells from mitomycin C-induced apoptosis mainly via suppressing the mitochondria-mediated intrinsic apoptosis pathway, but not in an extrinsic manner.

    Topics: Antibiotics, Antineoplastic; Apoptosis; bcl-2-Associated X Protein; Caspase 3; Caspase 9; Cell Death; Cell Line, Tumor; Cell Proliferation; Cell Survival; Cytoprotection; DNA Fragmentation; Dose-Response Relationship, Drug; Enzyme Activation; Formazans; Humans; L-Lactate Dehydrogenase; Melanoma; Membrane Potential, Mitochondrial; Mitochondria; Mitomycin; Molecular Structure; Silybin; Silymarin; Sirtuin 1; Tetrazolium Salts; Time Factors; Tumor Suppressor Protein p53

2009
Honeybee venom induces calcium-dependent but caspase-independent apoptotic cell death in human melanoma A2058 cells.
    Toxicon : official journal of the International Society on Toxinology, 2008, Aug-01, Volume: 52, Issue:2

    Honeybee (Apis mellifera) venom (BV) has been reported to exhibit anticancer effects, but its mode of action at the cellular and molecular levels remains largely unknown. We found that honeybee venom induced apoptosis in human melanoma A2058 cells but not in normal skin fibroblast Detroit 551 cells. The BV-induced apoptosis was accompanied by generation of reactive oxygen species and alteration of mitochondrial membrane potential transition. Treatment with antioxidants significantly attenuated BV-induced apoptosis. Although caspase-2 and -3 were slightly activated by BV, inhibitors of caspase-2 and -3 could not block BV-induced apoptosis in A2058 cells. Data from immunostaining indicated that EndoG and AIF were translocated from mitochondria to the cytosol or nucleus, suggesting that BV induces apoptosis in A2058 cells via a caspase-independent pathway. In addition, cJun N-terminal kinases (JNK) and ERK were rapidly activated after a 5 min incubation with BV, while p38 and AKT were inactivated after 30 min administration of BV. Inhibition of JNK significantly attenuated BV-triggered apoptotic death. Moreover, BV induced a rapid and marked increase in cytosolic calcium ion. Incubation of cells under calcium-free conditions effectively diminished BV-induced apoptosis. Furthermore, when the calcium-free treatment was combined with ouabain, the recovery of cellular calcium fluctuation protected A2058 cells against BV-induced apoptosis. Finally, treatment of A2058 cells with melittin, the major component of BV, resulted in similar elevation of calcium levels and cell killing effects, suggesting that melittin is the major determinant in BV-triggered cell death. These observations provide a molecular explanation for the antiproliferative properties of BV, and suggest that this agent may be useful in treating melanoma.

    Topics: Animals; Apoptosis; Bee Venoms; Bees; Calcium; Caspases; Cell Line, Tumor; Cell Survival; Cytosol; Dose-Response Relationship, Drug; Drug Screening Assays, Antitumor; Enzyme Activation; Enzyme Inhibitors; Extracellular Signal-Regulated MAP Kinases; Fibroblasts; Formazans; Humans; MAP Kinase Kinase 4; Melanoma; Melitten; Membrane Potential, Mitochondrial; Ouabain; Reactive Oxygen Species; Tetrazolium Salts

2008
Characterization of human angiogenin variants implicated in amyotrophic lateral sclerosis.
    Biochemistry, 2007, Oct-23, Volume: 46, Issue:42

    Human angiogenin (ANG), the first member of the angiogenin family (from the pancreatic ribonuclease A superfamily) to be identified, is an angiogenic factor that induces neovascularization. It has received much attention due to its involvement in the growth of tumors and its elevated expression level in pancreatic and several other cancers. Recently the biological role of ANG has been shown to extend to the nervous system. Mutations in ANG have been linked with familial as well as sporadic forms of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder characterized by selective destruction of motor neurons. Furthermore, mouse angiogenin-1 has been shown to be expressed in the developing nervous system and during the neuronal differentiation of pluripotent stem cells. We have now characterized the seven variants of ANG reported in ALS patients with respect to the known biochemical properties of ANG and further studied the biological properties of three of these variants. Our results show that the ribonucleolytic activity of six of the seven ANG-ALS implicated variants is significantly reduced or lost and some variants also show altered thermal stability. We report a significant reduction in the cell proliferative and angiogenic activities of the three variants that we chose to investigate further. Our studies on the biochemical and structural features of these ANG variants now form the basis for further investigations to determine their role(s) in ALS.

    Topics: Amyotrophic Lateral Sclerosis; Cell Line, Tumor; Cell Proliferation; Chromatography, High Pressure Liquid; Circular Dichroism; Enzyme Stability; Formazans; Genetic Variation; Humans; Melanoma; Models, Molecular; Molecular Weight; Mutation; Protein Denaturation; Protein Engineering; Protein Renaturation; Ribonuclease, Pancreatic; Temperature; Tetrazolium Salts

2007
Effects of several flavonoids on the growth of B16F10 and SK-MEL-1 melanoma cell lines: relationship between structure and activity.
    Melanoma research, 2002, Volume: 12, Issue:2

    Although flavonoids seem to be capable of acting at all stages of the carcinogenic process, little information is available on their action in melanoma cell lines. The aim of this study was to assess the response of B16F10 and SK-MEL-1 melanoma cell lines to treatment with six different flavonoids after 24 and 72 h of exposure and to relate the response to their structure. We then compared the findings with those for melphalan treatment. When cultures were treated for 24 h, only slight inhibition at the highest concentrations (25 and 50 microM) of tangeretin and luteolin were observed, whereas melphalan caused a dose-related inhibition of growth at all concentrations. Quercetin, hesperetin, 7,3'-dimethylhesperetin and eriodictyol did not produce any effect at 24 h on B16F10 or SK-MEL-1 cells, results which point to the low toxicity of flavonoids. After 72 h of exposure culture growth was inhibited by 7,3'-dimethylhesperetin at 50 microM, but lower concentrations had no effect. Tangeretin was the most effective of the flavonoids in inhibiting B16F10 and SK-MEL-1 cell growth, showing a clear dose-response curve after 72 h. These results suggest that the absence of the C2-C3 double bond on hydroxylated flavonoids results in a loss of effect on both the cell lines, while the higher activity of tangeretin compared with 7,3'-dimethylhesperetin suggests that the presence of at least three adjacent methoxyl groups confers a more potent antiproliferative effect.

    Topics: Animals; Cell Division; Cell Survival; Dose-Response Relationship, Drug; Flavonoids; Formazans; Humans; Melanoma; Melanoma, Experimental; Mice; Mice, Inbred C57BL; Skin Neoplasms; Structure-Activity Relationship; Tetrazolium Salts; Tumor Cells, Cultured

2002
Selective toxicity of 1-methyl-4-phenylpyridinium ion (MPP+) to pigmented melanoma cells in vitro.
    Anti-cancer drug design, 1991, Volume: 6, Issue:3

    Topics: 1-Methyl-4-phenylpyridinium; Formazans; Humans; In Vitro Techniques; Melanins; Melanoma; Oxidation-Reduction; Pigmentation; Tumor Cells, Cultured

1991
Cytotoxic effect of 1-methyl-4-phenylpyridinium ion on human melanoma cell lines, HMV-II and SK-MEL-44, is dependent on the melanin contents and caused by inhibition of mitochondrial electron transport.
    Biochemical medicine and metabolic biology, 1990, Volume: 44, Issue:1

    MPP+, an oxidative metabolite of a neurotoxin, MPTP, was found to be cytotoxic to human melanoma cell lines, HMV-II and SK-MEL-44. After 3 days of culture in the presence of MPP+, a larger amount of MPP+ was accumulated in HMV-II cells than in SK-MEL-44 cells, which correlated well with the melanin contents; HMV-II cells contain larger amounts of melanin than SK-MEL-44 cells. After 6 days of culture in the presence of MPP+, the cytotoxicity of MPP+ on these cell types was evaluated by counting cell numbers with the dye exclusion test and double-layer soft agar clonogenic assay. It was found that exposure to MPP+ reduced the survival of HMV-II cells more significantly than that of SK-MEL-44 cells. In HMV-II cells, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay was used to elucidate the mechanism of MPP+ lethality. The formazan formation was reduced markedly by the presence of MPP+ at concentrations much lower than those required for cell death. These results suggest that cytotoxicity of MPP+ may be ascribed to its accumulation due to high affinity for melanin, and to inhibition of the enzymes utilizing ubiquinone in the mitochondrial respiratory chain.

    Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Cell Line; Cell Survival; Colony-Forming Units Assay; Electron Transport; Formazans; Humans; Melanins; Melanoma; Mitochondria; MPTP Poisoning; Oxidation-Reduction; Pyridinium Compounds; Tumor Cells, Cultured

1990
Histochemical findings in different types of malignant melanoma: biological and clinical significance.
    Archives for dermatological research = Archiv fur dermatologische Forschung, 1975, Dec-10, Volume: 254, Issue:2

    By means of histochemical methods (gel-film incubation-media) superficial spreading melanoma, nodular melanoma and lentigo maligna melanoma are investigated. The result of this examination is that with regard to their enzyme spectra, the nodular melanoma and the nodular part of the superficial spreading melanoma are very similar. Glucose-6-phosphate dehydrogenase shows the strongest enzyme reaction, followed by succinate dehydrogenase and lactate dehydrogenase. The beta-hydroxybutyrate dehydrogenase reaction is always weak. The reaction of acid phosphatase is between negative and weakly positive. Significant differences, however, are observed in lentigo maligna and in lentigo maligna melanoma. In both, the strongest formazan deposits are seen with succinate dehydrogenase, sometimes also with lactate dehydrogenase. The glucose-6-phosphate dehydrogenase reaction, however, is sometimes considerably weaker. In the case of lentigo maligna melanoma, the activity of beta-hydroxybutyrate dehydrogenase often is increased, and acid phosphatase also shows higher reactions than in the other melanomas. These differences in the enzyme pattern correspond to the different biological behavior of the tumours. The enzymatical and biological characteristics of lentigo maligna melanoma possibly derive more from the characteristics of the tumour itself which are not dependent on the area.

    Topics: Acid Phosphatase; Esterases; Formazans; Glucosephosphate Dehydrogenase; Humans; Hydroxybutyrate Dehydrogenase; L-Lactate Dehydrogenase; Melanoma; Monophenol Monooxygenase; Nevus, Pigmented; Skin; Succinate Dehydrogenase

1975