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Biomedical subjects

M Terada

Publications and source records attributed to M Terada.

At least 541 records · Page 30Linked to original sources
PubMed1984

Angiostrongylus cantonensis: paralysis due to avermectin B1a and ivermectin.

Paralysis due to avermectin B1a and ivermectin of Angiostrongylus cantonensis was compared to that of phenylephrine (an alpha-adrenergic agonist) and strychnine (a cholinergic inhibitor). The paralyzing action of ivermectin (2.5 X 10(-9) g/ml) was inhibited by the single, simultaneous addition of picrotoxin (3 X 10(-5) M), whereas the effect of the drug (2.5 X 10(-7) g/ml) was reversed only when picrotoxin was given with cholinergic spasmogens such as pyrantel and eserine. Bicuculline (3 X 10(-5) M) had a similar antagonistic effect for picrotoxin, but bicuculline was less effective. The paralyzing action of avermectin B1a (3.6 X 10(-14) M, 3.0 X 10(-14) g/ml) was antagonized only when picrotoxin was given with cholinergic spasmogens such as pyrantel, eserine, and N-methylcytisine (N-MC), or alpha-adrenergic antagonists such as phentolamine and dibenamine. On the other hand, the paralyzing action of strychnine (3 X 10(-6) M) or phenylephrine (3 X 10(-5) M) was relatively uninfluenced by picrotoxin, but was antagonized by pyrantel and N-MC or dibenamine. These results suggest that a gabergic mechanism is involved in the paralyzing action of ivermectin, as well as avermectin B1a, in A. cantonensis.

Adrenergic alpha-Antagonists↗
PubMed1984

Mutagenicity of instant coffee on cultured Chinese hamster lung cells.

Coffee showed mutagenic activity in cultured Chinese hamster lung (CHL) cells as assessed by using diphtheria toxin resistance as a selective marker. Most of the mutagenicity was suppressed in the presence of sodium bisulfite. The contribution of methylglyoxal to the total mutagenicity of coffee was less than 3%.

Aldehydes↗
PubMed1984

Integration of v-rasH does not necessarily transform an immortalized murine cell line.

Plasmids containing v-rasH and Ecogpt were constructed, and used to transfect two established cell lines of mouse origin, NIH3T3 cells and m5S cells. After transfection, most NIH3T3 cells, which are resistant to mycophenolic acid, showed phenotypes characteristic of neoplastic transformation, whereas no mycophenolic acid-resistant m5S cells showed these phenotypes; integration of functionally intact v-rasH in immortalized murine cells is not sufficient for neoplastic transformation in m5S cells. The resistance to the transformation was probably due to a lower level of the v-rasH gene transcripts in m5S cells.

Animals↗
PubMed1984

Amplification of the c-myc oncogene in human stomach cancers.

Amplified c-myc oncogene was found in the DNAs of 2 of 11 human stomach cancers transplanted into nude mice; the amplification was 8- to 10-fold in one tumor and 13- to 15-fold in the other. Both tumors in which the c-myc oncogene was amplified were poorly differentiated adenocarcinomas, but there was no clear-cut correlation between the histological types or growth rates of the tumors and amplification of the c-myc oncogene. No amplification of the c-myc gene was detected in DNAs from 4 cultured stomach cancer cell lines, 19 primary stomach cancers or 11 metastases to lymph nodes from human stomach cancers.

Adenocarcinoma↗
PubMed1983

Mutagenic activity of heterocyclic amines in Chinese hamster lung cells with diphtheria toxin resistance as a marker.

The mutagenicities of 8 heterocyclic amines, which had been purified from pyrolysates of amino acids and proteins, broiled fish and fried beef, were assayed in Chinese hamster lung cells (CHL cells) in culture in the presence and absence of a metabolic activation system, with diphtheria toxin resistance as a selective marker. 3-Amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) was the most mutagenic of the heterocyclic amines tested. 3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ), 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-9H-pyrido[2,3-b]indole (A alpha C), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) and 2-aminodipyrido[1,2-a:3',2'-d]imidazole (Glu-P-2) showed mutagenic activity on CHL cells, their specific activities being in the order shown above. All the compounds except Trp-P-1 required the presence of a metabolic activation system for mutagenicity on CHL cells.

Amines↗
PubMed1983

Enhanced incorporation of radioactive inorganic phosphate into phospholipids of HeLa cells by tumor promoters.

Teleocidin, a new tumor promoter, increased incorporation of radioactive inorganic phosphate (32Pi) into phospholipids in HeLa cells. This effect was detected within 1 h on incubation of the cells in medium containing teleocidin. The half-maximum effective dose of teleocidin was approximately 10 ng/ml. The main effect of teleocidin was on the incorporation of 32Pi into the phosphatidylcholine fraction, with a lesser effect on 32Pi incorporation into other phospholipid fractions. Increased incorporation of 32Pi into phospholipids was also observed on incubation of the cells with 12-O-tetradecanoylphorbol-13-acetate (TPA), dihydroteleocidin B, or lyngbyatoxin A, which are all complete tumor promoters, and also with mezerein, which is an incomplete and second stage promoter. On the other hand, at concentrations of up to 1 microgram/ml, 4-O-methyl TPA and Ca2+ ionophore A23187, which are incomplete and first stage promoters, and phorbol, which has no promoting activity in skin carcinogenesis, did not cause any increased incorporation of 32Pi into phospholipid fractions of HeLa cells.

Alkaloids↗
PubMed1983

Enhancement of antitumor activity of bleomycin by benzamide in vitro and in vivo.

The cytotoxic effects of bleomycin on HeLa cells in culture were enhanced by incubation of the cells with benzamide, a potent inhibitor of poly(ADP-ribose) polymerase, at concentrations at which benzamide alone did not show any cytotoxicity. Benzamide plus bleomycin display enhanced therapeutic effects against Ehrlich ascites tumor cells in vivo. On daily treatment with various doses of bleomycin plus benzamide for 10 days, mice with Ehrlich ascites tumors survived longer than mice on treatment with bleomycin alone.

Animals↗
PubMed1983

Poly(ADP-ribose): structure, quantification, and biological significance.

We have been working on poly(ADP-Rib) since our discovery of it. This lecture will review recent findings on this polymer obtained in our laboratory. Poly (ADP-Rib) has long been thought to be a linear homopolymer attached to nuclear protein. The ribose-ribose bond of poly(ADP-Rib) was shown to be an alpha(1" leads to 2') ribosidic bond. There are two molecular forms of poly(ADP-Rib), namely low molecular weight (L) and high molecular weight (H) poly(ADR-Rib) molecules. The L and H fractions of poly(ADP-Rib) are separable by gel filtration, sucrose density gradient centrifugation and polyacrylamide gel electrophoresis. Physicochemically the L and H forms differ in their molecular size, solubility in high salt, rate of hydrolysis by venom phosphodiesterase and circular dichroism (CD) spectrum. However, the two forms have a similar ultraviolet (UV) absorption spectrum, both show a similar hyperchromicity on heating to 98 degrees C or hydrolysis with snake venom phosphodiesterase and give similar results on ordinary chain length determination. The great discrepancy in size observed by physicochemical methods and by the ordinary chain length method indicates the presence of a branching structure in poly(ADP-Rib). The branching structure was proved by demonstrating the presence of a unique compound, 2'[1"-ribosyl-2"(1"'-ribosyl)]adenosine-5',5",5"'-tris(phosphate) and by electron microscopy. The amount of poly(ADP-Rib) was determined by our new method, consisting of tritium labeling and high performance liquid chromatography. The merit of this method is that it can determine the recovery of poly(ADP-Rib) exactly and that its sensitivity is high. The amount of poly(ADP-Rib) changed dramatically when human promyelocytic leukemia cells were induced to differentiate by dimethyl sulfoxide or 12-O-tetradecanoylphorbol-13-acetate. The use of inhibitors of poly (ADP-Rib) polymerase in combination with bleomycin, a DNA damaging antitumor drug, potentiated the antitumor activity of bleomycin against Ehrlich ascites carcinoma cells in vivo.

Animals↗
PubMed1983

Induction of diphtheria toxin-resistant cells by mutagen-carcinogens.

A mutation assay system with Chinese hamster lung (CHL) cells in culture has been established using diphtheria toxin resistance as a phenotypic selection marker. The results of series of studies on this mutation assay system are summarized and presented. Dose-dependent increase in the number of diphtheria toxin-resistant (DTr) cells was observed when the cells were exposed to a mutagen-carcinogen and then incubated in fresh medium for an expression period of 7 to 8 days. After exposure to ethyl methanesulfonate, the number of DTr cells was much higher than the number of thioguanine-or ouabain-resistant cells. ADP-ribosylation of elongation factor 2 (EF-2) catalyzed by diphtheria toxin was measured in cell-free extracts from the parent cells and 17 DTr cells, including 6 spontaneous DTr cells and 11 DTr cells induced by mutagens; the numbers of ADP-ribose molecules transfer to EF-2 in extracts of mutant cells were less than 1% of that in extract of the parent cells. Various mutagen-carcinogens, including heterocyclic amines isolated from pyrolysates of amino acids, proteins, and broiled fish, have been assayed with this mutation assay system in the presence or absence of a metabolic activation system and the results of these studies are also presented. In addition, a method to detect DTr cells in situ has been developed using autoradiographic method. The potential usefulness of this method for detection of DTr cells with no proliferative capacity to form colony and for analysis of cellular events occurring after exposure of the cells to mutagen-carcinogens is discussed.

Adenosine Diphosphate Ribose↗
PubMed1983

Mutagenicity of nitropyrenes in Chinese hamster V79 cells.

The mutagenic effects of 1-nitropyrene, and 1,3- and 1,8-dinitropyrenes on Chinese hamster V79 cells in the presence or absence of X-irradiated Syrian hamster embryo cells were examined. Without Syrian hamster embryo cells, 1,3-dinitropyrene had weak mutagenic activity and 1,8-dinitropyrene had strong, dose-related mutagenic activity. With Syrian hamster embryo cells, the mutagenicities of both 1,3-and 1,8-dinitropyrenes were appreciably increased. 1-Nitropyrene did not induce ouabain-resistant mutants at concentrations of up to 10 micrograms/ml either with or without Syrian hamster embryo cells.

Animals↗