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Biomedical subjects

H Tsuda

Publications and source records attributed to H Tsuda.

At least 613 records · Page 34Linked to original sources
PubMed1983

Assessment of nitrosamine transplacental carcinogenesis in the Syrian golden hamster.

The effects of diethylnitrosamine (DEN) and vinylethylnitrosamine (VEN) in the F1 generation of Syrian golden hamsters are described after the compounds were administered to the P generation during the second half of pregnancy. Morphologic findings revealed that the upper respiratory tract (i.e., trachea) was most affected. VEN appeared highly effective because the first neoplastic alterations (papillary polyps) were seen in both the P and the F1 animals at the 30th postnatal day. The fetal tracheal epithelium also showed chromosomal aberrations after DEN exposure, and VEN enhanced the cloning efficiency of these cells. Combined in vivo - in vitro studies are discussed with special emphasis on the early detection of transformation and neoplastic growth.

Animals↗
PubMed1983

Digital ulcers/gangrene and immunoglobulin classes/complement fixation of anti-dsDNA in systemic lupus erythematosus patients.

The immunoglobulin classes/complement fixation of anti-dsDNA were studied in sera obtained from 17 systemic lupus erythematosus (SLE) patients with digital ulcers and/or gangrene (Group A); 13 SLE patients with leg ulcer, peripheral neuropathy or livedo (Group B); 24 SLE patients with Raynaud's phenomenon (Group C); and 18 SLE patients with active lupus nephritis (Group D). Antibodies to dsDNA of IgG and IgA classes were commonly present (often in high titers) in Groups A and D. However, complement fixation of anti-dsDNA was more common in Group D than in any of the other 3 groups.

Antibodies, Antinuclear↗
PubMed1983

Inhibitory effect of butylated hydroxyanisole and ethoxyquin on the induction of neoplastic lesions in rat liver after an initial treatment with N-ethyl-N-hydroxyethylnitrosamine.

The effect of butylated hydroxyanisole (BHA) and ethoxyquin (EQ) on hepatocarcinogenesis initiated with N-ethyl-N-hydroxyethylnitrosamine in rats was investigated. The results clearly demonstrated that BHA and EQ inhibited the development of gamma-glutamyltranspeptidase - positive foci, hyperplastic nodules and hepatocellular carcinomas in the rat system employed.

Animals↗
PubMed1983

Modification of chemical carcinogenesis by antioxidants.

The effects of the antioxidants, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), ethoxyquin (EQ), and sodium L-ascorbate (SA) on two stage chemical carcinogenesis were investigated in male F344 rats initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), N-ethyl-N-hydroxyethylnitrosamine (EHEN), N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) or N-methylnitrosourea (MNU). BHA was given in diet at a dose level of 0.5 or 2.0%, BHT at 1.0%, SA at 5.0% and EQ at 0.8% for 29-51 weeks. Complete autopsy was performed at sacrifice and organs were examined histologically for the presence of preneoplastic and neoplastic lesions. All of the antioxidants tested exerted a positive influence on the development of BBN- or MNU-initiated bladder carcinogenesis. Similarly, these chemicals tended to enhance the appearance of forestomach tumors although the data gained after BHT administration were not significant. In clear contrast, no effect was observed on glandular stomach carcinogenesis and, with the exception of SA, the antioxidants all showed inhibition of the development of preneoplastic and neoplastic lesions in the liver. EQ increased the occurrence of renal adenoma in EHEN-treated rats. Clear differences were observed with respect to the modification of thyroid carcinogenesis after MNU initiation, BHT demonstrating strong promotion activity whereas BHA and SA had no effect. Thus organ specificity, with regard to both direction of modification and to the effects of individual antioxidants was apparent, this intriguing finding offering hope for the development of future experimental approaches for elucidation of the mechanisms underlying chemical carcinogenesis.

Animals↗
PubMed1983

Organ-specific promoting effect of phenobarbital and saccharin in induction of thyroid, liver, and urinary bladder tumors in rats after initiation with N-nitrosomethylurea.

Tumor-promoting effects of phenobarbital (PB) and sodium saccharin (SS) were tested in rats pretreated with N-nitrosomethylurea (NMU) with special reference to the site of their action. Male F344 rats were initially given injections of NMU (20 mg/kg i.p.) twice a week for 4 weeks, then given basal diet containing 0.05% PB or 5% SS for the next 32 weeks, and then killed. Appropriate control studies were also done. Histological examination of whole organs of the rats showed that PB promoted thyroid carcinogenesis whereas SS did not. A significant increase in the incidences of total tumors as well as papillary adenocarcinoma of the thyroid was observed in the group given PB after NMU (p less than 0.001). The incidence of papillary adenoma with or without papillary adenocarcinomas was also high in the NMU-PB-treated group. The organ-specific promoting effect of PB in the induction of preneoplastic lesions, as demonstrated by development of gamma-glutamyl transpeptidase-positive foci in the liver and of SS in papillary or nodular hyperplasia in the urinary bladder, as reported previously, was also confirmed. The incidences of papillomas in the forestomach were similar in groups treated with NMU-PB, NMU-SS, or NMU alone. The results indicate that PB is a tumor promoter in the liver and thyroid and that SS is a tumor promoter in the urinary bladder of rats.

Adenocarcinoma, Papillary↗
PubMed1982

Chromosomal aberrations in tracheal epithelial cells of the fetal Syrian golden hamster after transplacental N-diethylnitrosamine administration.

Transplacental effect of N-diethylnitrosamine (DEN) on chromosomal morphology, was investigated in fetal tracheal epithelium of Syrian hamsters. At the 15th day of pregnancy, Syrian golden hamsters were injected subcutaneously with a tumorigenic dose of DEN (50, 100 and 200 mg/kg body wt). Two hours later, the fetal tracheae were isolated, epithelial cells of the respiratory mucosa were separated from mesenchymal tissue and were transferred to cell culture. At 24, 48 and 72 h after cultivation, chromosomal damages were examined. The results showed clearly that a high incidence of chromosomal aberrations, particularly chromatid-type exchanges, were seen in the epithelial cells from DEN-treated groups.

Animals↗
PubMed1982

Route-dependent, organ-specific effects of carcinogens on induction of hyperplastic liver nodules in rats.

The inductions of hyperplastic liver nodules (HN) by four carcinogens were examined by their administration continuously and repeatedly by intragastric (i.g.), intraperitoneal (i.p.), intravenous (i.v.) and/or subcutaneous (s.c.) injections before (initiation stage) or after (promotion stage) exposure to N-2-fluorenylacetamide (2-FAA) in male F344 rats. Diethylnitrosamine (DEN), a water-soluble hepatocarcinogen, and 3'-methyl-4-dimethylaminobenzene (3'-Me-DAB), a water-insoluble hepatocarcinogen, markedly increased development of HN when administered by any route in both stages. However, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), a water-soluble non-hepatocarcinogen, and benzo[a]pyrene (B[a]P), a water-insoluble non-hepatocarcinogen, increased HN slightly by all or some of the routes of application only in the initiation stage. The influence of the administration route was more evident with water-insoluble compounds in the promotion stage and with non-hepatocarcinogens in the initiation stage.

2-Acetylaminofluorene↗
PubMed1982

Relationship between phagocytosis and immunoglobulin A release from human colostral macrophages.

Macrophages and neutrophils that contain mainly secretory immunoglobulin A (IgA) comprise the majority of cells in human colostrum. These cell populations were separated and analyzed for their ability to release total IgA and secretory IgA when stimulated to phagocytose. Colostral macrophages phagocytosed opsonized bacteria and nonopsonized latex particles; at the same time, IgA was released. Neutrophils poorly phagocytosed opsonized bacteria but actively phagocytosed latex particles. In contrast to the macrophages, the neutrophils did not release IgA, even after active phagocytosis of latex. Consequently, colostral macrophages are the main source of IgA released from colostral leukocytes when these cells are exposed to organisms or particles that are phagocytosed. A function for colostral neutrophils which sequester IgA is proposed.

Adolescent↗
PubMed1982

IgD-plasma cell leukemia associated with pyroglobulinemia and pyroglobulinuria. New types of pyroglobulin and cytoplasmic fibrils.

New pyroglobulin variants were found in a patient with a typical plasma cell leukemia. One was found in the urine and proved to be a variant of Bence-Jones' protein with a molecular weight of approximately 68,000. The other was found in the serum and appears to be the myeloma protein of IgD. Furthermore, an ultrastructural study disclosed myeloma cells in both peripheral blood and bone marrow to have cytoplasmic fibrils which might be unique for plasma cell leukemia.

Bence Jones Protein↗
PubMed1982

Induction of hyperplastic liver nodules in hepatectomized rats treated with 3'-methyl-4-dimethylaminoazobenzene, benzo[a]pyrene or phenobarbital before or after exposure to N-2-fluorenylacetamide.

The effects of pre- and post-administration of 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), benzo[a]pyrene (B[a]P), and phenobarbital (PB) on the induction of hyperplastic liver nodules by N-2-fluorenylacetamide (2-FAA) were studied in F344 rats. Rats were given 3'-Me-DAB (0.06% in the diet), B[a]P (80 mg/kg b.wt. x 7, intragastrically) or PB (0.05% in the diet) for 6 weeks before (experimental series I) or after (experimental series II) diet containing 0.02% 2-FAA for 2 weeks, and killed in week 10 of the experiment. The number and total area of hyperplastic nodules per unit area of liver were greatest in rats treated with 3'-Me-DAB in both experimental series. B[a]P significantly increased the induction of hyperplastic nodules in experimental series I and PB significantly increased it in experimental series II. Partial hepatectomy performed during administration of test chemicals enhanced the induction of hyperplastic nodules, especially in experimental series I, and an oral dose of carbon tetrachloride during 2-FAA feeding enhanced it in both experimental series. In the present system, initiating activity of both the hepato- and the non-hepatocarcinogen was detected, and promoting activity of both the hepatocarcinogen and the hepatopromoter was demonstrated.

2-Acetylaminofluorene↗
PubMed1982

Changes in activities of uridine diphosphate-glucuronyltransferases during chemical hepatocarcinogenesis.

Changes in the activities of hepatic uridine diphosphate-glucuronyltransferases (UDP-GTs) were investigated during the induction of hyperplastic nodules (enzyme-altered foci) by a system consisting of diethylnitrosamine (DEN) followed by N-2-fluoroenylacetamide (FAA) and including partial hepatectomy. The activity of the late fetal form of UDP-GT, which was assayed towards o-aminophenol (o-GT activity), was induced rapidly by a single ip injection of DEN (200 mg/kg) or 3-methylcholanthrene (40 mg/kg) or by the continuous administration of FAA (0.02% in diet) alone. This activity further increased with the appearance of the nodules, while the activity of the neonatal form, which was assayed toward phenolphthalein (p-GT activity) and was inducible by phenobarbital, increased only slightly. The increased o-GT activity showed a good correlation with the increased number or area of enzyme-altered foci detected by gamma-glutamyltransferase activity staining, but the p-GT activity did not, though it was significantly increased. In hyperplastic nodules and well differentiated hepatomas induced by DEN (0.1% in drinking water, 3 weeks) but isolated long after cessation of DEN, o-GT activity was markedly increased, but p-GT activity was decreased or remained at the level of normal rat liver. These data indicate that the increased o-GT activity may be one of the enzyme markers for preneoplastic hepatic cells. An antioxidant, butylated hydroxyanisole (BHA) (0.75% in diet), markedly elevated the hepatic o-GT activity rapidly after being administered with FAA in the above system, and the induction of the nodules was inhibited.

2-Acetylaminofluorene↗
PubMed1982

Carcinogenic effect of carbazole in the liver of (C57BL/6N x C3H/HeN)F1 mice.

The carcinogenic effect of carbazole (9H-carbazole) in (C57BL/6N X C3H/HeN)F1 (B6C3F1) mice was examined. Groups of 50 mice of both sexes were given a basal diet containing 0.6, 0.3, or 0.15% carbazole for 96 weeks and were then placed on an unsupplemented basal diet until they were killed at week 104. Mice surviving longer than 52 weeks were included in effective numbers. Significant increases in the induction of neoplastic lesions were found in the livers and forestomachs of mice given carbazole as compared to the control groups. The lesions in the livers were classified into two types, neoplastic nodules or hepatocellular carcinomas. The incidences of both types of lesions were almost 100% in mice treated with carbazole, and both types of lesions were significantly increased in all mice except the males given 0.6% carbazole in their diet. The incidences of hepatocellular carcinomas were in general higher than those of neoplastic nodules. Though not statistically significant, increased incidences of pulmonary metastases were found in the groups given carbazole. Significantly increased incidences of neoplastic lesions and papillomas in the forestomach in all groups of female and male mice were also noted in the mice fed 0.6% carbazole. Squamous cell carcinoma induction was significantly different in male mice given 0.6% carbazole as compared to controls. These results indicate that carbazole is carcinogenic to the liver and forestomach in B6C3F1 mice and suggest that carbazole may be an environmental carcinogen relevant to cancer risk in humans.

Animals↗