Search PubMed⌕ Search

Biomedical subjects

M Takahama

Publications and source records attributed to M Takahama.

83 records · Page 5Linked to original sources

Primary osteogenic sarcoma of pulmonary artery.

A 44-year-old woman was hospitalized for nonproductive cough. Chest roentogenogram revealed a calcified nodular mass at the right hilum. The patient was treated as tuberculosis of the hilar lymph node, however, her symptoms exacerbated within a year. A tumor obstructing the right main stem bronchus was demonstrated on bronchofiberscopic examination. Thoracotomy was carried out and tumor was diagnosed as primary osteogenic sarcoma of the pulmonary artery by pathological examination of the resected specimen. There was no clinical finding of osteogenic sarcoma throughout the bones.

Adult↗

Induction of apoptosis by dopamine in human oral tumor cell lines.

Dopamine dose-dependently reduced the viable cell number of both human salivary gland tumor HSG and oral squamous cell carcinoma HSC-2, HSC-4, and NA cells. CoCl2 significantly reduced both the cytotoxic activity and radical intensity of dopamine (determined by ESR spectroscopy). Dopamine produced DNA fragments (demonstrated by TUNEL method) and induced degradation of cytokeratin by activated caspase in HSG cells (detected by an immunocytochemical method, using a specific M30 monoclonal antibody). FACS analysis demonstrated that dopamine induced DNA fragmentation, a biochemical hallmark of apoptosis, in human promyelocytic leukemia HL-60 cells. The addition of catalase did not prevent the apoptosis-inducing activity of dopamine, reducing the possibility of the involvement of H2O2 for dopamine-induced apoptosis. Dopamine transiently induced p38 mitogen-activated protein kinase (MAP kinase) phosphorylation. However, an inhibitor of p38 MAP kinase phosphorylation, SB203680, failed to inhibit the dopamine-induced apoptosis. These data suggest that p38 phosphorylation at an early stage may not be a causative event for apoptosis.

Apoptosis↗

Inhibition by Porphyromonas gingivalis LPS of apoptosis induction in human peripheral blood polymorphonuclear leukocytes.

Many factors, such as cytokines and bacterial products, are known to affect the life-span of polymorphonuclear leukocytes (PMNs). We investigated here whether Porphyromonas gingivalis (P.gingivalis) LPS slows down the apoptotic process of PMNs. During incubation in regular culture medium, the viability of PMNs progressively declined, producing apoptotic cells, characterized by chromatin condensation, internucleosomal DNA fragmentation, cell shrinkage and blebbing of plasma membrane. P.gingivalis LPS significantly increased the viability of PMNs and reduced the production of fragmented DNA, as efficiently as E.coli LPS. The present study suggests that the retardation of PMNs apoptosis by P.gingivalis LPS may modulate the restoration of acute inflammation in the periodontal tissues, where activated PMNs accumulate.

Apoptosis↗

Radical intensity and cytotoxic activity of curcumin and gallic acid.

Natural phenolic compounds, curcumin and gallic acid, were compared for their cytotoxic activity in relation to their radical modulating activity. These two compounds induced apoptotic cell death in human promyelocytic leukemic HL-60 cells and human oral squamous carcinoma HSC-4 cells. Curcumin was more cytotoxic than gallic acid. Catalase reduced significantly the cytotoxic activity of gallic acid, but not that of curcumin. ESR spectroscopy demonstrated that curcumin produced radicals under alkaline conditions, scavenged the superoxide anion radical, and enhanced the radical intensity of sodium ascorbate at higher concentrations. As compared with curcumin, gallic acid produced higher amounts of radicals and more efficiently scavenged the superoxide anion radical. Gallic acid reduced the radical intensity of sodium ascorbate, suggesting a possible interaction between these two compounds. These data suggest that curcumin and gallic acid induce apoptosis by different mechanisms.

Antineoplastic Agents↗

Amino acid utilization during cell growth and apoptosis induction.

The amino acid utilization between human promyelocytic leukemia (HL-60), human oral squamous carcinoma (HSC-2, HSC-4, NA), human salivary gland tumor (HSG) and rat neuron cells (PC-12) were compared, using amino acid analyzer. All these cells consumed four essential amino acids (valine, methionine, isoleucine, leucine), glutamine and arginine, whereas they produced glycine, alanine and ammonia, without significantly affecting threonine, tyrosine, phenylalanine, histidine or lysine concentration. Serine and glutamine utilization varied considerably from cell to cell. HL-60 cells consumed serine and arginine at much higher rates than other cells. Serine depletion accumulated the G1 arrested cells, and produced increasing numbers of the apoptotic cells. Supplementation of serine significantly extended the period of logarithmic cell growth. During apoptosis induction of HL-60 cells by dopamine, sodium ascorbate or sodium 5,6-benzylidene-L-ascorbate, the oxidation of methionine to methionine sulfoxide was enhanced, but the consumption of serine, glutamine and arginine was reduced. In the presence of HL-60 cells, the methionine oxidation was significantly inhibited, suggesting the antioxidant action of the cells. These present study suggests the importance of re-evaluation of culture condition for each cell lines.

Amino Acids↗

Role of hydrogen peroxide in cytotoxicity induction by ascorbates and other redox compounds.

Role of hydrogen peroxide (H2O2) in the induction of cytotoxicity by ascorbic acid derivatives was investigated. Ascorbic acid derivatives which produced radicals (sodium 5,6-benzylidene-L-ascorbate (SBA), sodium-L-ascorbate, D-isoascorbic acid) dose-dependently reduced the viable cell number of human squamous carcinoma (HSC-2, HSC-4, NA), human salivary gland tumor (HSG) and human promyelocytic leukemia (HL-60) cell lines. Conversely, L-ascorbic acid-2-phosphate magnesium which did not produce radicals, was inactive. This suggests the possible role of the ascorbate radical in apoptosis induction. The cytotoxic activity of SBA was partially reduced by catalase, and the extent of inhibition by catalase was considerably different, depending upon which target cells were used. On the other hand, the cytotoxic activity of sodium ascorbate, isoascorbic acid, hydrogen peroxide and gallic acid was more effectively inhibited by catalase. These data suggest that mechanisms other than H2O2 might be involved in the induction of cytotoxicity by SBA.

Antineoplastic Agents↗