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T Sugimura

Publications and source records attributed to T Sugimura.

At least 685 records · Page 38Linked to original sources
PubMed1984

Carcinogenicity in mice of mutagenic compounds from glutamic acid and soybean globulin pyrolysates.

2-Amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole and 2- aminodipyrido [1,2-a:3',2'-d]imidazole, potent mutagens from glutamic acid pyrolysate, were given orally to CDF1 mice of both sexes at concentrations of 0.05% in pellet diet. 2-Amino-3-methyl-9H-pyrido[2,3-b]indole and 2-amino-9H-pyrido[2,3-b]indole, potent mutagens from soybean globulin pyrolysate, were given to CDF1 mice of both sexes at concentrations of 0.08%. Hepatocellular carcinomas and hemangioendothelial sarcomas in the brown adipose tissue were induced in high incidence by all these compounds.

Animals↗
PubMed1984

Carcinogenicity in mice of a mutagenic compound, 2-amino-3-methylimidazo[4,5-f]quinoline, from broiled sardine, cooked beef and beef extract.

A potent mutagenic compound, 2-amino-3-methylimidazo-[4,5-f]quinoline (IQ), isolated from broiled sardines, cooked beef and beef extract was tested for carcinogenicity in CDF1 mice of both sexes. Mice were given diet containing 0.03% IQ or control diet for up to 675 days. Tumors were observed mainly in the liver, forestomach and lung. In the mice given IQ, the incidences of these tumors were as follows: liver tumors - 41% in males and 75% in females; tumors of the forestomach - 41% in males and 31% in females; lung tumors - 69% in males and 42% in females. In the control mice, incidences of these tumors were as follows: liver tumors - 9% in males and 8% in females; tumors of the forestomach - 3% in males and 0% in females; lung tumors - 21% in males and 18% in females. The incidences of tumors in the liver, forestomach and lung were significantly higher in mice given IQ than in control mice.

Animals↗
PubMed1984

Detection of pX proteins in human T-cell leukemia virus (HTLV)-infected cells by using antibody against peptide deduced from sequences of X-IV DNA of HTLV-I and Xc DNA of HTLV-II proviruses.

A 41-kilodalton protein was detected in four human T-cell leukemia virus type I (HTLV-I)-infected cell lines, a 68-kilodalton glycoprotein in MT-2 cells, and a 38-kilodalton protein in an HTLV-II-infected cell line by using antibody against a synthetic dodecapeptide, a portion of the polypeptide deduced from the nucleotide sequence of the X regions of HTLVs.

Animals↗
PubMed1984

Nucleotide sequence analysis of human T-cell leukemia virus type II.

The total nucleotide sequence of an infectious clone of human T-cell leukemia virus type II (HTLV-II) provirus was determined. The provirus has 8,952 nucleotides with a long terminal repeat (LTR) at each end. The LTR consists of 341 +/- 1 bases of U3, 248 +/- 1 bases of R, and 201 bases of U5 regions. There are gag, pol, and env coding frames in this order from the 5' end of the provirus as in other avian or mammalian retroviruses. A coding frame that can code 178 amino acid residues found between gag and pol is supposed to be for a protease that hydrolyses a gag precursor protein to matured gag proteins. The gag and protease genes and the pol and env genes, respectively, partly overlap. In the region termed X between env and 3' LTR, there are three major open reading frames. Oligopeptides deduced from the sequence of one of the open reading frame in HTLV-I were synthesized chemically, and antibodies against these peptides were raised in rabbits. With these antibodies, 41 kdalton and 38 kdalton proteins were detected in cells infected with HTLV-I and HTLV-II, respectively.

Base Sequence↗
PubMed1984

Induction of cancers in the intestine, liver and various other organs of rats by feeding mutagens from glutamic acid pyrolysate.

The mutagenic compounds 2-amino-6-methyldipyrido[1,2-alpha:3',2'-d]imidazole (Glu-P-1) and 2- aminodipyrido [1,2-alpha: 3',2'-d]imidazole (Glu-P-2), which were isolated from a glutamic acid pyrolysate and are potent carcinogens in the liver and brown adipose tissue of mice, were found to be multipotent carcinogens in rats. These compounds were each given to F344 rats of both sexes at a concentration of 500 ppm in pellet diet for up to 24 months. Glu-P-1 induced tumors in the colon, small intestine, liver, Zymbal gland, clitoral gland and brain. Glu-P-2 produced tumors in the same sites at slightly lower incidence. The multipotent carcinogenicities of Glu-P-1 and Glu-P-2 in rats and mice suggest that heterocyclic amines present in cooked food may be important in the development of human cancer.

Adenocarcinoma↗
PubMed1984

Pseudotype viruses bearing envelope antigens of Japanese isolates of human T-cell leukemia viruses type I.

We tried to transmit human T-cell leukemia virus type I (HTLV-I) into non-lymphoid cells and found that S+L- CCC cat cells were permissive for HTLV-I. Using these HTLV-positive cat cells, vesicular stomatitis virus (VSV) pseudotypes bearing envelope antigens of Japanese isolates of HTLVs were prepared and their reactivities with human or rabbit serum were examined. Japanese HTLV2M, HTLV10Y, and HTLVMT-2 pseudotypes and American HTLVPL pseudotype were neutralized by sera of Japanese and American patients with adult T-cell leukemia/lymphoma (ATL) and rabbit antisera against HTLV. Each serum showed similar antibody titers against different pseudotypes. Thus, envelope antigens of four HTLVs that reacted with the human and rabbit sera were considered to belong to a single serotype.

Animals↗
PubMed1984

A monoclonal antibody reactive with gastric carcinoma.

A monoclonal antibody reactive with gastric carcinomas of the stomach was established. This antibody reacted with 88% (15/17) of the scirrhous carcinomas, and 75% (6/8) of the well differentiated adenocarcinomas of the stomach tested, but did not react with normal gastric mucosa or various other normal tissues, with the exception of the mucosa of the large intestine.

Adenocarcinoma↗
PubMed1984

Presence of 1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acids and tyramine as precursors of mutagens in soya sauce after nitrite treatment.

Soya sauce showed marked direct-acting mutagenicity toward Salmonella typhimurium TA 100 after nitrite treatment. Three precursors showing mutagenicity after nitrite treatment were isolated from soya sauce. Their structures were determined to be (-)-(1S,3S)-1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid [(-)-(1S,3S)-MTCA], its stereoisomer (-)-(1R,3S)-MTCA and tyramine. The numbers of revertants of TA 100 induced by 1 mg each of (-)-(1S,3S)-MTCA, (-)-(1R,3S)-MTCA and tyramine, after nitrite treatment, were 17 400, 13 000 and 3 900, respectively, without S9 mix. The amounts of MTCA isomers and tyramine in various Japanese soya sauces showing mutagenicity after nitrite treatment were 82-678 and 17-2 250 micrograms/mL, respectively. Most soya sauces produced in the USA showed weaker mutagenicity than those produced in Japan and contained lower, if not undetectable, amounts of the three precursors of mutagens. The mutagenicity of MTCA isomers and tyramine accounted for 16-61 and 1-35%, respectively, of the mutagenicity of the soya sauces after nitrite treatment. The mutagen(s) produced from (-)-(1S,3S)-MTCA with nitrite was a minor product(s), the major product being the non-mutagen, (-)-(1S,3S)-1-methyl-2-nitroso-1,2,3,4-tetrahydro-beta-carboline-3-carbo xylic acid [(-)-(1S,3S)-MNTCA], but the mutagen 4-(2-aminoethyl)-6-diazo-2,4-cyclohexadienone, produced from tyramine with nitrite, was one of the major products.

Carbolines↗
PubMed1984

Demonstration of carcinogenicity in F344 rats of 2-amino-3-methyl-imidazo[4,5-f]quinoline from broiled sardine, fried beef and beef extract.

The mutagenic compound 2-amino-3-methylimidazo[4,5-f]quinoline, originally isolated from broiled sardines and also present in cooked beef and beef extract, is being tested for carcinogenicity in F344 rats of both sexes. High incidences of tumors of the Zymbal gland, colon, small intestine and liver in males have been observed in the first 300 days of the experiment.

Adenocarcinoma↗
PubMed1984

Amplification and over-expression of the c-myc gene in Morris hepatomas.

Morris hepatoma 7794A was found to have its c-myc gene amplified 5- to 10-fold. The over-expression of c-myc was observed in all three hepatomas studied (Morris hepatomas 5123D, 7136A and 7794A), although in the first two instances the c-myc genes were not amplified. Over-expression or deregulation of c-myc seems to be a general phenomenon associated with hepatoma.

Animals↗
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↗
PubMed1984

Kinetics of nitrosation of thioproline, the precursor of a major nitroso compound in human urine, and its role as a nitrite scavenger.

The kinetics of nitrosation of thioproline was studied. The rate of the reaction increased with decrease in pH, and was first-order with respect to nitrite concentration. The reaction rate was proportional to the concentration of total thioproline (free plus protonated), not to that of free thioproline. The initial reaction rate followed the equation: rate = k4 X [thioproline] X [NaNO2] X [H+] The rate constant was found to be 49.4M-2 . sec-1 at pH 2.0 and 37 degrees. Thioproline acted as a nitrite scavenger, and suppressed the formation of a carcinogen, N-nitroso-N-benzylmethylamine, from N-benzylmethylamine and nitrite. More than 90% of the formation of N-nitroso-N-benzylmethylamine was inhibited by adding 20mM thioproline to a reaction mixture containing 20mM N-benzylmethylamine and 20mM sodium nitrite at pH 3.0 and 37 degrees.

Antineoplastic Agents↗
PubMed1984

Study of the promoting effect of sodium chloride on gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine in inbred Wistar rats.

The effect of sodium chloride on the promotion stage of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was studied in male inbred Wistar rats. Rats in group I were given MNNG at a concentration of 50 micrograms/ml in their drinking water for 12 weeks and then 1 ml of saturated NaCl solution intragastrically once a week until experimental week 65. Rats in group II were given MNNG for 12 weeks and then 1 ml of distilled water intragastrically once a week until week 65. Rats in group III were not treated for the first 12 weeks and were then given 1 ml of saturated NaCl solution intragastrically once a week until week 65. The incidence of adenomatous hyperplasias in the glandular stomach was significantly higher in group I than in group II, but the incidences of gastric adenocarcinomas and adenomas in groups I and II were not significantly different. No neoplastic or preneoplastic changes were observed in the stomach in group III.

Adenocarcinoma↗