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T Sugimura

Publications and source records attributed to T Sugimura.

1,103 records · Page 62Linked to original sources
PubMedDate not supplied

Chronic administration of the mutagenic heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine induces cardiac damage with characteristic mitochondrial changes in Fischer rats.

Fischer-344 rats of both sexes were administered the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) for 52 wk at the dietary level of 400 ppm. Light microscopic and ultrastructural investigation of the myocardium revealed prominent changes in all PhIP-treated male and female animals investigated. These were characterized by a diffuse proliferation of markedly enlarged mitochondria, with abundant cristae and often containing lamellar bodies as inclusions. PhIP is well known to cause DNA adducts in the rat heart, and there are numerous reports of mutations in mitochondrial DNA in both humans and experimental animals being associated with very similar lesions to those observed in the present study. The results thus suggest that this heterocyclic amine induces cardiac damage by the same mechanism.

Animals↗
PubMedDate not supplied

Increased serum soluble IL-2 receptor levels following interferon therapy in patients with chronic hepatitis C.

BACKGROUND/AIMS: To clarify whether the response of host cellular immunity to IFN therapy can be an indicator of efficacy, we monitored serum levels of soluble IL-2 receptor (sIL2R) before and after IFN therapy. METHODOLOGY: Serum sIL2R levels before and after interferon therapy were monitored in 53 patients with chronic hepatitis C. Natural Interferon(IFN)-alpha, 9 MU/day (everyday for 2 weeks followed by 3 times/week for 22 weeks), was administered to all patients. RESULTS: After the IFN therapy, sIL2R levels were significantly increased (before, 403.4+/-221.1 U/mL, and after, 542.0+/-307.6 U/mL, p<0.01). The patients were divided into two groups: the complete response (CR) group who were negative for serum hepatitis C virus (HCV)-RNA 6 months after the therapy, and the recurrence group who were positive for HCV-RNA 6 months after the therapy. Between these two groups, sIL2R levels before therapy were not significantly different, and sIL2R levels after therapy were also not significantly different. Although the ratio of sIL2R levels before and after was monitored, there was no significant difference between the CR group and recurrence group ((sIL2R after IFN)/(sIL2R before IFN)): 1.39+/-0.65 in the CR group and 1.99+/-2.07 in the recurrence group). CONCLUSIONS: sIL2R increased due to IFN administration, but it is not a good indicator for the efficacy of IFN therapy. It seems that the response of cellular immunity to IFN therapy does not play an important role in its efficacy.

Adult↗
PubMedDate not supplied

Evaluation of a selective prostaglandin E receptor EP1 antagonist for potential properties in colon carcinogenesis.

BACKGROUND: Cyclooxygenases (COXs) and prostanoids play pivotal roles in colon carcinogenesis. This study was designed to determine the chemopreventive effects of ONO-8711, a selective prostaglandin E receptor EP1 antagonist, on the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) in male F344 rats and to compare its potential with that of nimesulide, a well-documented selective COX-2 inhibitor. MATERIALS AND METHODS: Five-week-old male F344 rats received s.c. injections of AOM (15 mg/kg body weight) or the saline vehicle once weekly for two weeks and were fed the control diet (AIN-76A) or the experimental diets containing 400 or 800 ppm of ONO-8711 or 400 ppm nimesulide for 5 weeks. RESULTS: Administration of ONO-8711 at 800 ppm significantly reduced the total number of ACF/colon and 5-bromodeoxyuridine (BrdUrd) labeling index as compared to the control diet group (by 31% and 66%, respectively). As expected, dietary administration of nimesulide also suppressed the development of ACF and BrdUrd labeling index in the colon, by about 39% and 54%, respectively. CONCLUSION: Our finding that ONO-8711 significantly suppresses colonic ACF formation and cell proliferation strengthens the hypothesis that the selective prostaglandin E receptor EP1 antagonists possesses chemopreventive activity against colon cancer development.

Animals↗
PubMedDate not supplied

Experimental gastric cancer.

Since Sugimura and Fujimura (1967) succeeded in selectively inducing gastric carcinomas in rats by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (1), similar models for the induction of gastric carcinomas in other species by using MNNG and its ethyl derivative N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) have been established. The susceptibility to gastric carcinogenesis, the histologic types of gastric carcinomas induced, and their biological behavior depend on the mode of treatment, species, strain and/or sex. The organ specificity of MNNG correlates well with the level of DNA methylation in target and non-target tissues following oral administration in rats. The high concentration of methylated DNA bases in the stomach mucosa appears to result from thiol-mediated acceleration of the decomposition of MNNG. Experimental gastric carcinogenesis is markedly modified by various factors and agents, including bile reflux, bile acids, sodium chloride, and ulceration, indicating that both host and environmental factors contribute significantly to gastric carcinogenesis by chemical carcinogens.

Animals↗