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Biomedical subjects

Y Tagawa

Publications and source records attributed to Y Tagawa.

At least 217 records · Page 12Linked to original sources
PubMed1987

Lesions of the prostate glands and seminal vesicles induced by N-methylnitrosourea in F344 rats pretreated with ethinyl estradiol.

In an attempt to induce a high incidence of prostate carcinoma, N-methylnitrosourea (MNU), a multipotential carcinogen, was given during the period of cell proliferation of the prostate gland induced by administration of methyltestosterone (MT) to F344 rats pretreated with ethinyl estradiol (EE). Rats were given diet containing EE for 3 weeks and then diet containing 300 ppm of MT for 5 days. On the 3rd day of MT-treatment, they were given a single intravenous injection of 50 mg/kg body wt. of MNU. Control rats (group 4) were given vehicle only. After treatment with MT for 5 days, the rats were given basal diet (group 1), diet containing MT (group 2) or diet periodically containing EE (groups 3 and 4) until the end of the experiment (week 60). Carcinoma of the prostate was found only in 1 of 17 rats in group 3. Atypical hyperplasia of the prostate was found in 1 of 10 rats in group 1 and 3 of 17 rats in group 2. The incidences of atypical hyperplasia of the seminal vesicles in groups 1-3 were 0%, 41% and 29%, respectively. No tumor promoting effect of MT or EE was observed except promotion by MT on the development of atypical hyperplasia of the seminal vesicles.

Animals↗
PubMed1987

Proliferative response of rat accessory sex organs to dietary sex hormones after castration or initial dietary administration of estrogen.

The hormone dependent proliferative response of five accessory sex organs was examined subsequent to castration-induced or estrogen-induced atrophy using male six-week-old F344 rats. Three weeks after castration, rats were treated with dietary methyltestosterone (300 ppm), ethinyl estradiol (0.75 ppm) or methyltestosterone plus ethinyl estradiol for up to 17 days. Cell proliferation was assessed by 3H-thymidine incorporation as determined from labelling indices using autoradiography. The maximum labelling indices which appeared on days 2 or 3 of administration of methyltestosterone were 24.3, 8.4, 9.6, 21.6 and 13.7% for the ventral, lateral and dorsal prostate, seminal vesicle and coagulating glands, respectively. Combined methyltestosterone and ethinyl estradiol induced mild proliferative responses whereas ethinyl estradiol did not. In a further group of non-castrated rats which were pretreated with dietary ethinyl estradiol for three weeks and then given methyltestosterone, the maximum labelling indices were about 70 to 80% of that in castrated rats.

Animals↗
PubMed1987

[Changes in the cell cycle and RNA content of cultured cancer cells treated with actinomycin D].

For the purpose of reasonable evaluation of the cell kinetics of RNA synthesis inhibitors, the flow cytometric technique using acridine orange staining for simultaneous measurement of cellular DNA and RNA content was applied in order to analyze the effects of actinomycin D (ACT-D) on cultured cancer cells (PC1). ACT-D 0.05 microgram/ml, a dose that produced little inhibitory effect on the growth curve, led to G1 accumulation after the appearance of G2M, and a decrease in RNA content was concomitantly observed at 48-72h, although the RNA level had nearly recovered to normal at 120 h. On the other hand, ACT-D 0.1 microgram/ml, a dose that produced a significant inhibitory effect, resulted in the initiation of G1-phase accumulation, a maximal peak of G2M accumulation and a decrease in RNA content at 48 h, after which there was a tendency toward G1-phase accumulation and a marked decrease in RNA content which continued for 120 h. Such a marked decrease in RNA content coincided with high values of the G1a X G1b ratio in the G1 phase. These results suggest that ACT-D has an inhibitory action on the cell cycle between G1a and G1b, accompanying a marked decrease in RNA content.

Carcinoma, Squamous Cell↗
PubMed1986

Comparison of the effects of 13 phenolic compounds in induction of proliferative lesions of the forestomach and increase in the labelling indices of the glandular stomach and urinary bladder epithelium of Syrian golden hamsters.

Groups of 6-week-old male Syrian golden hamsters were given 13 different phenolic compounds for 20 weeks. Of these compounds, 2(3)-tert-butyl-4-methoxyphenol (BHA), 2-tert-butyl-4-methylphenol (TBMP) and p-tert-butylphenol (PTBP) strongly induced hyperplasia and tumorous lesions in the forestomach. Catechol, p-methylphenol (PMYP), p-methoxyphenol (PMOP), caffeic acid, methylhydroquinone (MHQ) and pyrogallol were less active, and resorcinol, hydroquinone, propylparabene and tert-butylhydroquinone (TBHQ) were not active. The labelling index in the forestomach epithelium was significantly increased by addition to the diet of BHA, TBMP, catechol, PMOP, PTBP and MHQ. PMOP induced epithelial damage and regenerative hyperplasia of the pyloric region. Catechol, caffeic acid and PMYP induced similar though less marked lesions. The labelling index in the glandular stomach was significantly increased by oral catechol (P less than 0.05) or PMOP (P less than 0.05). No histopathological lesions were observed in the urinary bladder epithelium, but propylparabene (P less than 0.05), catechol, TBHQ and MHQ increased the labeling index. These findings indicate that PTBP and TBMP may be carcinogenic for hamster forestomach after long-term administration, and that both one hydroxy and tert-butyl substituents may be important for induction of hamster forestomach tumors.

Animals↗
PubMed1986

Induction of prostate carcinoma in situ at high incidence in F344 rats by a combination of 3,2'-dimethyl-4-aminobiphenyl and ethinyl estradiol.

Male F344 rats were given a diet containing 0.75 ppm of ethinyl estradiol for 3 weeks and a basal diet for 2 weeks alternately 10 times, and 2 days after each change to basal diet (on the third day of feeding of the basal diet), a single s.c. injection of 50 mg/kg body weight of 3,2'-dimethyl-4-aminobiphenyl. Then they were given the basal diet until week 60 and sacrificed for histological examination. Prostatic carcinomas were found in 18 of 21 rats (85.7%) after this treatment but in only 1 of 19 rats (5.2%) maintained on normal diet throughout the experiment but given 3,2'-dimethyl-4-aminobiphenyl at the same times as the diet given to test rats. All the carcinomas were microscopic and developed in the ventral lobe of the prostate. This method may ultimately lead to a useful animal model of prostatic carcinoma.

Aminobiphenyl Compounds↗