Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human neutrophil-mediated oxidative processes against a human hepatoma cell line, HCC-M, was visualized at the cellular level by using a silicon-intensified target camera and subsequently processing with a computer-assisted digital-imaging processor. Neutrophils were activated by a streptococcal preparation, OK-432. A hydroperoxide-sensitive tracer, dichlorofluorescein diacetate, was loaded in HCC-M and temporal and spatial changes of lipid peroxides in this cell after addition of stimulated neutrophils were analyzed. The luminol-dependent chemiluminescence activity of neutrophils was significantly enhanced and continued for at least 2 hr by stimulation with OK-432, and its activity was shown to be accumulated at the site where a neutrophil attached with HCC-M. The intensity of dichlorofluorescein fluorescence in HCC-M rapidly increased after adding stimulated neutrophils, and their reaction was significantly attenuated by superoxide dismutase. The number of non-viable cells was increased as the dichlorofluorescein fluorescence increase. It is suggested that oxidative stress may play an important role in neutrophil-mediated tumor-cell damage.
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PMID:Visualization of oxidative processes at the cellular level during neutrophil-mediated cytotoxicity against a human hepatoma cell line, HCC-M. 131 29

Tumor cells (AH130 hepatoma cell originated from rat) were injected intraportally into Donryu rats to produce liver metastases 21 days later. Phagocyte cells activity was depressed by the administration of Silica, which significantly increased the number of surface liver metastases. Phagocyte cells were stimulated by beta 1-3-glucan, which significantly reduced the number of metastases. And the administration of free radical scavenger (SOD, Catalase) increased the number of metastases. Non parenchymal cells (NPC) of the liver play a main role of self defence line for portally liver metastases. Then free radical from these cells were noticed in this study. NPC were isolated, from pronase perfused rat liver. O2- production by activated NPC was measured by chemiluminescence with CLA. NPC activated by beta 1-3-glucan added sera increased the luminescence of CLA, and SOD depressed the production of chemiluminescence. SOD activity of hepatocytes and tumor cells (AH130) were measured by NBT methods. Hepatocytes had high potential production of SOD, in contrast AH130 had poor production. These results suggest that free radicals from liver NPC was important for protecting liver metastases.
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PMID:[The effect of free radicals from non-parenchymal cells (NPC) of the liver on the development of liver metastases in rat]. 823 83

The metabolic changes in rat hepatoma cell line, AH70 cells, after coculturing with Kupffer cells were visualized using a silicon-intensified target camera and subsequent processing with a computer-assisted digital imaging processor. In cocultured tumor cells, nonactivated Kupffer cells reduced mitochondrial energization as indicated by the decrease in the fluorescence intensity of rhodamine 123 (Rh123) and induced lipid peroxidation as shown by the dichlorofluorescein (DCF) activation. The reduction in Rh123 could be eliminated by addition of an analogue of L-arginine (NG-monomethyl-L-arginine), suggesting the involvement of nitric oxide (NO.) in the decrease in mitochondrial energization. Superoxide dismutase did not inhibit the reduction in Rh123 but significantly inhibited DCF activation. These findings indicate that the latter reaction was mediated by superoxide anion. Two h after the cells were cocultured, propidium iodide-positive, severely injured tumor cells significantly increased in number. This increase was significantly attenuated by addition of NG-monomethyl-L-arginine but not by superoxide dismutase, suggesting that NO. may be greatly involved in Kupffer cell-mediated injury of AH70 cells. In another set of experiments, the culture medium of Kupffer cells caused no significant alteration of Rh123, DCF, and propidium iodide-associated fluorescences in AH70 cells. In addition, ultrastructural observation revealed that the membrane-to-membrane attachment between Kupffer cells and tumor cells occurred within 30 min after coculturing. These results suggest that Kupffer cell-derived NO. release, triggered by the close contact with tumor cells, may induce damage to tumor cells via inhibition of mitochondrial energization.
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PMID:Nitric oxide mediates Kupffer cell-induced reduction of mitochondrial energization in hepatoma cells: a comparison with oxidative burst. 838 20

The metabolic changes in a rat hepatoma cell line, AH70 cells, after co-culture with rat Kupffer cells (KC) were visualized and analysed using a fluorescence microscope equipped with a silicon intensified target camera and a laser scanning confocal microscopic system. Kupffer cells were isolated from male Wistar rats, and cultured without any stimuli. The non-activated KC reduced the mitochondrial energization in the cocultured AH70 cells within 2 h, which was indicated by decreased rhodamine 123 (Rh123) fluorescence. Either NG-monomethyl-L-arginine or dexamethasone significantly attenuated the KC-induced mitochondrial dysfunction in AH70 cells, suggesting the involvement of nitric oxide (NO) derived from inducible-type nitric oxide synthase (iNOS). Administration of monoclonal antibody (mAb) directed against rat ICAM-1 also prevented the decrease in Rh123 fluorescence. Electron microscopy revealed that the membrane-to-membrane attachment between KC and AH70 cells occurred within 2 h. A laser scanning confocal microscopic observation using mAb against ICAM-1 presented that the ICAM-1 expression on AH70 cells and KC increased after the co-culture. It is therefore concluded that the KC-mediated mitochondrial dysfunction of hepatoma cells largely depends on NO production by iNOS. Furthermore, the present study supports a scenario that the NO production and release from KC is triggered by the close contact with hepatoma cells through adhesion molecules such as ICAM-1.
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PMID:Nitric oxide mediates mitochondrial dysfunction in hepatoma cells induced by non-activated Kupffer cells: evidence implicating ICAM-1-dependent process. 858 48

N,N-Dimethylformamide (DMF) affects cellular differentiation, causes hepatotoxicity and gastric irritation, and may be carcinogenic. Since these processes involve changes in cellular pH homeostasis, we investigated the effects of DMF on H+ extrusion and cytosolic pH (pHi) of mouse hepatoma cells (Hepa 1C1C7). Extracellular pH was monitored using a silicon-based sensor system (Cytosensor microphysiometer) and pHi was monitored by fluorescence spectrophotometry. Superfusion of cells with DMF (0.25 to 0.5 M) suppressed the extracellular acidification rate (ECAR) below baseline. Following washout of DMF there was a rapid, concentration-dependent, prolonged overshoot of ECAR above baseline rates. Removal of extracellular Na+ or superfusion with amiloride abolished the overshoot in acidification rate, indicating involvement of Na+/H+ exchange. The overshoot was dependent on extracellular glucose, suggesting that it arises from an increase in metabolic acid production. Fluorescence measurements showed that DMF did not change pHi. Furthermore, DMF did not alter the rate of pHi recovery of cells acid loaded using nigericin, indicating that DMF does not directly alter Na+/H+ exchange activity in these cells. In summary, these data suggest that suppression of acidification rate by DMF is likely due to decreased metabolic acid production. Washout of DMF is then accompanied by increased glucose metabolism and H+ efflux via Na+/H+ exchange. It is possible that alterations in H+ production and transport contribute to the hepatotoxicity of DMF and its effects on cellular differentiation.
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PMID:N,N-Dimethylformamide modulates acid extrusion from murine hepatoma cells. 987 85

The quaternisation of N-substituted benzimidazoles by heating with various alkyl, allyl, propargyl and benzyl chlorides and bromides leads to the formation of benzimidazolinium salts. The interaction of N-monosubstituted benzimidazoles with various salts (CuCl2, ZnCl2, CoCl2, PdCl2 and AgNO3) yielded stable solid complexes. Potential cytotoxic activity of synthesised benzimidazolinium salts and benzimidazole metal complexes was tested in vitro on four monolayer tumour cell lines: MG-22A (mouse hepatoma), HT-1080 (human fibrosarcoma), B16 (mouse melanoma), Neuro 2A (mouse neuroblastoma) and normal mouse fibroblast cells. A preliminary analysis of the structure-activity relationship for the benzimidazole derivatives clearly indicates that the character of substituents in the benzimidazole ring has strong influence on the cytotoxic activity. The insertion of the silicon atom into the N-alkyl chain increases the cytotoxic activity of benzimidazolinium salts significantly, which show a very significant potency in vitro against all studied tumour cell lines, being particularly active in experiments with B16 (mouse melanoma). TD50 for the most active compounds are in the range 0.001-0.008 microg x ml(-1). Cytotoxicity of benzimidazole metal complexes (L2MX2) strongly depends on the metal nature. 1-(3-trimethylsilylpropyl)benzimidazole in dose 1 mg x kg(-1) inhibits carcinoma S-180 tumour growth by 62% (on ICR mice).
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PMID:Synthesis and antitumour activity of trimethylsilylpropyl substituted benzimidazoles. 1152 41

A novel series of silicon(IV) phthalocyanines substituted axially with one or two 1,3-bis(dimethylamino)-2-propoxy group(s) have been prepared by ligand substitution and alkoxy exchange reactions. Two dicationic and tetracationic phthalocyanines have also been prepared by methylation of two of these compounds. The nonionic phthalocyanines are essentially nonaggregated in common organic solvents and show a weak fluorescence emission, while the methylated derivatives are also nonaggregated, even in aqueous media, and exhibit a strong fluorescence emission. These new phthalocyanines, in particular the unsymmetrical and amphiphilic analogues, are highly potent against HepG2 human hepatocarcinoma cells and J774 mouse macrophage cells with IC50 values down to 0.02 microM. The photodynamic activities are related to the cellular uptake and the efficiency to generate singlet oxygen. A higher positive charge at the phthalocyanine hinders the uptake, reflected by the lower intracellular fluorescence intensity. Fluorescence microscopic studies have also revealed that the unsymmetrical phthalocyanine SiPc[C3H5(NMe2)2O](OMe) (4) has a high and selective affinity to the mitochondria of HepG2 cells.
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PMID:New amphiphilic silicon(IV) phthalocyanines as efficient photosensitizers for photodynamic therapy: synthesis, photophysical properties, and in vitro photodynamic activities. 1537 81

The interactions of four novel silicon(IV) phthalocyanines (SiPc), namely SiPc[OC(3)H(5)(NMe(2))(2)](2) (1), SiPc[OC(3)H(5)(NMe(2))(2)](OMe) (2), {SiPc[OC(3)H(5)(NMe(3))(2)](2)}I(4) (3), and {SiPc[OC(3)H(5)(NMe(3))(2)](OMe)}I(2) (4) with human serum albumin (HSA), bovine serum albumin (BSA), and maleylated bovine serum albumin (mBSA) were studied by fluorescence spectroscopy. The fluorescence emission of the serum albumins was effectively quenched by these phthalocyanines mainly through a static quenching mechanism. The higher Stern-Volmer quenching constants for the unsymmetrically substituted phthalocyanines 2 and 4 suggested that they have a stronger interaction with these proteins than the symmetrically substituted analogues 1 and 3. A series of non-covalent BSA or mBSA conjugates of these phthalocyanines were also prepared and evaluated for their in vitro photodynamic activity against HepG2 human hepatocarcinoma cells. The bioconjugation could enhance the photocytotoxicity of 1 and 4 by up to eight folds, but the effects on 2 and 3 were negligible. The results could be partly explained by two counter-balancing effects, namely the enhanced uptake and increased aggregation tendency of phthalocyanine due to BSA conjugation. As shown by absorption spectroscopy, the tetracationic phthalocyanine 3 was significantly aggregated in the protein cavity and its photocytotoxicity remained the lowest among the four photosensitizers.
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PMID:Preparation and in vitro photodynamic activity of novel silicon(IV) phthalocyanines conjugated to serum albumins. 1641 11

To increase the field of view for large objects in phase-contrast X-ray imaging, a large monolithic X-ray interferometer has been fabricated using an available silicon ingot of diameter 10 cm. A performance study of this interferometer has been carried out using a synchrotron X-ray source. The view size of the interference pattern obtained with this interferometer was 25 mm wide and 15 mm high and its visibility was 79%. Various structures of a sliced human hepatocellular carcinoma were identified as necrosis, hemorrhagic necrosis, normal liver tissue and blood vessel. The performance of this interferometer was sufficient for phase-contrast X-ray imaging.
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PMID:Phase-contrast X-ray imaging with a large monolithic X-ray interferometer. 1660 8

We describe a novel multicellular spheroid culture system that facilitates the easy preparation and culture of a spheroid microarray for the long-term monitoring of cellular activity. A spheroid culture device with an array of pyramid-like microholes was constructed in a silicon chip that was equipped with elastomeric microchannels. A cell suspension was introduced via the microfluidic channel into the microstructure that comprised silicon microholes and elastomeric microwells. A single spheroid can be formed and localized precisely within each microstructure. Since the culture medium could be replaced via the microchannels, a long-term culture (of approximately 2 weeks) is available on the chip. Measurement of albumin production in the hepatoma cell line (HepG2) showed that the liver-specific functions were maintained for 2 weeks. Based on the cellular respiratory activity, the cellular viability of the spheroid array on the chip was evaluated using scanning electrochemical microscopy. Responses to four different chemical stimulations were simultaneously detected on the same chip, thus demonstrating that each channel could be evaluated independently under various stimulation conditions. Our spheroid culture system facilitated the understanding of spheroid formation, culture, and viability assay on a single chip, thus functioning as a useful drug-screening device for cancer and liver cells.
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PMID:A multicellular spheroid array to realize spheroid formation, culture, and viability assay on a chip. 1698 97


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