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Biomedical subjects

M Morimoto

Publications and source records attributed to M Morimoto.

At least 379 records · Page 21Linked to original sources
PubMed1981

Gilvocarcins, new antitumor antibiotics. 1. Taxonomy, fermentation, isolation and biological activities.

Gilvocarcin V and gilvocarcin M, a group of antitumor antibiotics with a novel skeleton, were discovered in culture broths of Actinomycete DO-38. The producing organism, subsequently determined to be a new species and named Streptomyces gilvotanareus (NRRL 11382). Gilvocarcin V and M were isolated by ethyl acetate extraction and chromatography on silica gel. The antibiotics are active against Gram-positive bacteria and experimental tumors such as mouse sarcoma 180 and mouse leukemia P388.

Actinomyces↗
PubMed1981

Gilvocarcins, new antitumor antibiotics. 3. Antitumor activity.

Gilvocarcin V, isolated rom a Streptomyces culture showed activity against experimental tumors such as sarcoma 180, Ehrlich carcinoma, Meth 1 fibrosarcoma, MH134 hepatoma and lymphocytic leukemia P388. In particular, 40% of treated mice survived for 60 days, after intraperitoneal administration of gilvocarcin V to mice bearing Ehrlich ascites carcinoma. But it was marginally active against B16 melanoma and did not produce prolongation of lifespan of mice bearing Lewis lung carcinoma.

Aminoglycosides↗
PubMed1981

Antitumor activity of 7-n-(p-hydroxyphenyl)-mitomycin C in experimental tumor systems.

The antitumor activity of 7-N-(p-hydroxyphenyl)-mitomycin C (M-83) was compared with that of mitomycin C (MMC) in rodent tumor systems. M-83 exhibited more potent activity than MMC against the ascitic form of lymphocytic leukemia P388 and fibrosarcoma Meth 1, and doses of over 5 mg/kg of M-83 (1/6 LD50) resulted in some 60-day survivors. The chemotherapeutic ratio (optimal dose/MED) of M-83 was around 64 and was estimated to be approximately 5 to 8 times higher than that of MMC. Upon intravenous administration, M-83 also gave a better survival and showed a higher chemotherapeutic ratio than MMC against intravenously implanted P388. M-83 inhibited the growth of solid form of sarcoma 180 to the same extent as MMC at an equivalent dose, but showed a higher safety margin than MMC. M-83 was as effective as MMC against Lewis lung carcinoma at dose levels giving the same degree of toxicity. In vitro studies on tumor growth inhibition demonstrated that the cytotoxic effects of M-83 against leukemia P388 and fibrosarcoma Meth 1 cells were similar to and stronger than those of MMC, respectively.

Animals↗
PubMed1981

Comparison of the hematologic toxicity of 7-N-(p-hydroxyphenyl),-mitomycin C and mitomycin C.

7-N-(p-Hydroxyphenyl)-mitomycin C (M-83), a new analog of mitomycin C (MMC) with equivalent or greater antitumor potencies against various experimental tumors, was investigated to determine its hematologic toxicity in mice. M-83 showed a significantly lower toxicity than MMC with respect to myelosuppression and leukopenia when compared at equivalent effective doses. In M-83-treated mice, the damage to the bone marrow was much milder at the nadir point and the recovery from myelosuppression to the normal level was faster as compared with that in the case of MMC. As a result, the number of white blood cells in the peripheral blood of the M-83-treated groups was considerably greater than that in the MMC-treated ones. These findings suggest that M-83 may be effective in clinical use.

Animals↗
PubMed1980

Studies on antitumor activity of prumycin. II. Studies on distribution and excretion of prumycin.

Tissue distribution, excretion and metabolism of prumycin in normal mice and rats were studied by microbiological assay. Following the injection of prumycin into mice, high activity was detected and continued for 24 hours in the kidney, and the activity was also high in the skin, uterus, bone, liver, lung and stomach in this order. But concentration in the brain, heart, spleen and testis were too low to detect even 5 minutes after the injection. Prumycin was not inactivated by a variety of tissue homogenates in vitro. Therefore, inability to detect activity of prumycin in the spleen and testis appears to result from poor distribution rather than inactivation by these organs. About 70% of injected prumycin was excreted into rat urine in 24 hours but it was not detectable in feces. When prumycin was injected intravenously into dogs at the dose over 10 mg/kg, vomiting was observed in all animals, and LD50 was about 50 mg/kg.

Amino Sugars↗
PubMed1980

Studies on antitumor activity of prumycin. III. Mode of action of prumycin on HeLa S-3 cells.

The mode of action of prumycin was investigated using synchronized and asynchronous cultured HeLa S-3 cells. Prumycin inhibited significantly the growth of HeLa S-3 cells at the concentration over 5 mcg/ml. DNA synthesis as well as protein synthesis was strongly inhibited at the concentration of 10 mcg/ml of prumycin, but RNA synthesis was not inhibited by the same concentration. Prumycin did not block the transition of the cells from M phase to G1 phase, however, G2 phase cells were blocked clearly by this antibiotic.

Amino Sugars↗
PubMed1980

Studies on antitumor activity of prumycin. IV. Effect of prumycin on mouse immune system.

The effect of prumycin on the mouse immune system was studied. Prumycin at a dose of 75 mg/kg (1/2LD50) showed essentially no suppression of hemolytic plaque forming cells (PFC) against sheep red blood cells (SRBC) when it was administered on day 0, 1 or 2. However, a weak suppression was observed by administration of prumycin on day 3. Also a remarkable suppression of PFC was demonstrated when mouse spleen cells were pre-incubated with prumycin at the concentration over 62.5 mg/kg in vitro. The delayed-type hypersensitivity reaction against SRBC was remarkably suppressed by cyclophosphamide, but it was not much by prumycin, except by administration on the day of elicitation. Prumycin of a high concentration inhibited an uptake of 3H-thymidine by mouse spleen lymphocytes incubated with or without phytohemagglutinin, but that of a low concentration, 1.9 approximately 0.03 mcg/ml, slightly increased the blastogenic stimulation of lymphocytes.

Amino Sugars↗
PubMed1980

The mode of action of nanaomycin A in Gram-positive bacteria.

The mode of action of nanaomycin A on Gram-positive such as Staphylococcus aureaus, Bacillus cereus and Streptococcus faecalis was investigated. Nanaomycin A inhibited the biosyntheses of protein, DNA, RNA and cell-well peptidoglycan to a similar extent. It increased the oxygenous respiration of S. aureus cells at the minimal inhibitory concentration. The cells preincubated with nanaomycin A showed stimulation of proton influx after addition of N,N'-dicyclo-hexylcazrbodiimide, an inhibitor of Ca++, Mg++-ATPase. Nanaomycin A seems to interfere with the cytoplasmic or to inhibit coupling of oxidative phosphorylation, followed by secondary inhibitory effect on protein, nucleic acids and cell-wall peptidoglycan biosyntheses.

Anti-Bacterial Agents↗
PubMed1980

Tetrocarcins, novel antitumor antibiotics. II. Isolation, characterization and antitumor activity.

Novel antitumor antibiotics, tetrocarcin complex composed of three components (A, B and C) were isolated from the culture broth of Micromonospora chalcea KY11091 through various procedures. Tetrocarcins showed marked activity against experimental tumors such as mouse sarcoma 180 and mouse leukemia P388. Multiple injections showed better therapeutic effect against tumors. Mode of action of tetrocarcin A against Bacillus subtilis was found to be through the inhibition of RNA synthesis.

Aminoglycosides↗