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T Imazawa

Publications and source records attributed to T Imazawa.

At least 91 records · Page 5Linked to original sources
PubMed1990

[Effects of crude soybean trypsin inhibitor on pancreatic atrophy induced by BOP treatment in hamsters].

Experiment I: Female Syrian golden hamsters were given 5 weekly sc injections of N-nitrosobis (2-oxopropyl)amine (BOP) while simultaneously being treated with SBTI diet for 5 weeks (BOP+ SBTI). Other two groups were treated with BOP or SBTI alone. Sacrificed at week 30, the numbers of both adenocarcinomas and dysplastic lesions were decreased in the BOP+SBTI group relative to the BOP alone group. Experiment II: Female hamsters were given 3 weekly sc injections of BOP and then fed a SBTI diet for 40 weeks. The numbers of dysplastic lesions was decreased in the BOP and SBTI group relative to the BOP alone group. An inhibitory effect was observed for the pancreas in hamsters fed SBTI after BOP treatment. In experiments I and II, atrophic changes of pancreatic exocrine tissues and fatty tissue infiltration were observed in hamsters treated with BOP. The ratios of exocrine atrophy in pancreas sections were measured with the aid of an image processor. Areas (2.4 mm2) of splenic and gastric lobes were selected randomly, and the included exocrine tissue measured to allow calculation of percentage area of exocrine tissue atrophy. In hamsters simultaneously treated with BOP and SBTI, the percent areas of intact exocrine tissues in both splenic and gastric lobes were significantly higher (87% and 83%) as compared to the BOP group values (61% and 61%), at the level of p < 0.01, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1990

[Ultrastructural localization of myelin bodies and acid phosphatase activities in the liver and kidney induced by quinacrine in rats].

Electron microscopic studies were conducted to reveal the ultrastructural aspects of the myelin body and acid phosphatase activity in rats induced by quinacrine, an antimalarial drug. Each of 22 rats in three groups were examined. The first group of control rats was initially given a single i.p. dose (200 mg/kg) of diethylnitrosamine (DEN) only and then fed a CRF-1 basal diet for 8 weeks. The second and third group were treated with DEN or saline, and starting 2 weeks later, were fed a CRF-1 basal diet supplemented with 500 ppm quinacrine for 6 weeks. All animals were subjected to a partial hepatectomy at week 3, and then sacrificed at week 8. Liver and kidney tissues specimens from 2 rats per group were collected for routine electron microscopic study. Furthermore, the activity of acid phosphatase, a key enzyme for lysosomal activity, was also investigated. In this study, tissues were fixed with a solution of 2.5% glutaraldehyde in 0.1 M sodium cacodylate buffer. After fixation, tissues were frozen and their 8 microns sections were treated with Gomori's lead nitrate buffer solution, and post-fixed with a 1% osmium solution. After being embedded in Epon 812, ultrathin sections were made. Intracellular myelin bodies were observed in the hepatocytes, interlobular bile duct cells, renal glomerular podocytes and renal tubular cells in the quinacrine treated groups, but not were observed in rats treated with DEN alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid Phosphatase↗
PubMed1990

[Twenty-eight day repeated dose toxicity test of dicyclopentadiene in F344 rat].

A twenty-eight day repeated dose toxicity test of dicyclopentadiene (DCPD) was carried out in male and female F344 rats at the dose levels of 200, 40, 8 or 0 mg/kg/day. Thirty six animals of both sexes were divided into 6 groups of equal number. All groups were treated i.g. administration for 28 days daily, and two groups of them, at the dose levels of 200 and 0 mg/kg, were used for investigation of recovery. Inhibition of body weight gain was observed in the 200 mg/kg groups in both sexes and the 40 mg/kg group in male, but in female this inhibition was recovered at day 17 of the treatment. Increases in liver and adrenal gland weights, and decrease in thymus weight were noted in the 200 mg/kg groups in both sexes, and increase in kidney weight was also observed in the 200 and 40 mg/kg groups in male. On histopathological examination, hypertrophy of the adrenal cortex, and foamy cytoplasm in hepatocytes were observed in the 200 mg/kg groups of both sexes. Repair of histopathological lesions occurred within 14 days resting period. Based on these findings, it was concluded that the No Observed Effect Level of DCPD would be 8 mg/kg/day.

Administration, Oral↗
PubMed1989

[Application of BrdU-immunohistochemistry and lanthanum-tracer methods to the pathological evaluation of 1,3-dinitrobenzene testicular toxicity].

The pathogenesis of 1,3-dinitrobenzene (1,3-DNB)-associated testicular toxicity was investigated in Sprague-Dawley rats with 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry and lanthanum-tracer methods as well as routine histopathological examination. Animals were killed at 8, 12, 24, 48 and 96 hr after a single oral administration of 1,3-DNB at a dose of 25 mg/kg. Histopathologically, severe alterations in the testes such as degenerating pachytene spermatocytes and giant cell formation were observed by 24 hr. Immunohistochemical analysis revealed no differences in the distribution of BrdU-positive cells between treated and control rats throughout the experiment. Thus it was concluded that 1,3-DNB exerted no effects on DNA synthesis in spermatogonia and preleptotene spermatocytes. Using the lanthanum-tracer method, it was shown that although lanthanum could penetrate the intercellular space from the basement membrane, the tight junction, consisting of fusions of contiguous Sertoli cell membranes, prevented further diffusion in both control rats and those killed at 8 hr after dosing. On the other hand, at 24 hr after dosing, lanthanum penetrated into the adluminal compartment beyond the tight junctions, thus demonstrating loss of integrity of the blood-testis barrier. The results suggested that the Sertoli cell is the primary target of 1,3-DNB testicular toxicity.

Administration, Oral↗
PubMed1989

[Analysis of renal calcification and stone formation in rats treated with ethoxyquin using X-ray analytical scanning electron microscopy: ultrastructural observations and element analysis].

Rat renal calcification and stone formation were investigated using a JEOL-JSM840A scanning electron microscope (SEM) equipped with a LINK-QX200J energy dispersed X-ray detector (EDX). Male Wistar rats were treated with 100 ppm N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the drinking water or 10% NaCl in the diet for 8 weeks, and subsequently administered a dietary supplement of 0.1% ethoxyquin (EQ) for 32 weeks. An additional group received the EQ treatment alone. Calcification and stones were observed from the renal papilla to the pelvis region in all EQ treated groups. The incidence and grade of the lesion in the combined treated groups were much more greater than in the group treated with exposed to EQ alone. Ultrastructurally, microvilli on the surface of the renal papilla cells appeared degenerated or disappeared completely in the treated groups. Chemical element analysis of the renal stones revealed P and Ca to be the primary constituents. They were therefore considered to be of hydroxyapatite type.

Animals↗
PubMed1989

[Effect of vitamin A deficiency on PNUR-induced carcinogenesis in the rat upper digestive tract].

The effects of vitamin A (VA) deficiency on 1-propyl-1-nitrosourethan (PNUR)-induced tumorigenesis in the upper digestive tract were investigated in male F344 rats. Starting at 6 weeks old, animals were given PNUR in the drinking water (200 ppm) for one week, and starting 2 weeks later, were divided into 3 groups (30 rats/group) and maintained on VA-deficient diet, VA-supplemented diet (semipurified diet) or standard diet (CRF-1), respectively. An additional control group (10 rats) was fed VA-deficient diet without PNUR treatment. The experiment was terminated at 41 weeks after the beginning of PNUR administration, and development of tumors in the upper digestive tract was determined histopathologically. Squamous cell tumors were observed in the oral cavity, tongue and forestomach of all PNUR treated groups, while no tumors developed in the control group. Significantly higher incidences of forestomach papillomas were observed in the groups administered VA-deficient or VA-supplemented diets, as compared with that receiving standard diet (p less than 0.01, p less than 0.05, respectively). These results thus suggest that the higher incidences of forestomach tumors were probably due to general dietary differences (semipurified vs. standard diets) and not to the VA deficiency per se.

Animals↗
PubMed1988

Promoting effect of peroxisome proliferators in two-stage rat renal tumorigenesis.

A two-stage rat renal tumorigenesis model was employed to examine the promoting effects of peroxisome proliferators in the kidney. Groups of 20 male F344 rats were given 0.05% N-ethyl-N-hydroxyethylnitrosamine (EHEN) orally for the first 2 weeks as the initiator. Subsequently they were treated with clofibrate, simfibrate or di(2-ethylhexyl)phthalate (DEHP), respectively, at dietary concentrations of 0.35%, 0.35% and 1.2% for 24 weeks and killed for microscopical examination of the kidney. The incidences of renal cell tumors (RCT) and the numbers of RCT/kidney in rats given DEHP after initiation were significantly increased as compared to the controls. On the other hand, renal promoting effects were not evident in groups given clofibrate or simfibrate. Under the condition of this study, DEHP was found to act as a renal promoter.

Animals↗
PubMed1987

Relationship between the duration of treatment and the incidence of renal cell tumors in male F344 rats administered potassium bromate.

In order to ascertain the minimum induction time, minimum treatment period and total dose required for development of renal cell tumors, KBrO3 at a concentration of 500 ppm was administered in the drinking water to a total of 232 male F344 rats divided into 14 experimental groups and the development of tumors was examined by two different approaches. In a continued-treatment study, administration of KBrO3 was stopped at week 13, 26, 39, 52 or 104 and rats were immediately sacrificed for comparison with controls given distilled water (DW) alone. Renal cell adenomas were found as early as after 26 weeks of treatment with KBrO3. The yields of dysplastic foci, adenomas and adenocarcinomas of the kidney, follicular cell tumors of the thyroid and mesotheliomas of the peritoneum increased with treatment, the final incidences all being statistically significant after administration of KBrO3 for 104 weeks. To examine the effect of discontinued treatment, on the other hand, the rats were given KBrO3 for the first 13, 26, 39 or 52 weeks and were subsequently maintained on DW alone until sacrifice at week 104. The incidences of tumors in these groups were compared with that of a group continuously administered KBrO3 for 104 weeks. The yields of renal dysplastic foci, adenomas and adenocarcinomas in all discontinued-treatment groups were approximately equal to or even higher than those in the group given KBrO3 continuously for 104 weeks. It is concluded that, under the conditions of this study: the minimum induction time for the development of renal adenomas was 26 weeks and the minimum treatment period and total dose for the induction of renal adenomas and adenocarcinomas were 13 weeks and 4 g/kg, respectively, when the rats were maintained thereafter on DW for 2 years.

Animals↗
PubMed1986

Long-term in vivo carcinogenicity study of nalidixic acid in CDF1 mice.

Nalidixic acid (NA), a drug used for the treatment of urinary-tract infections, was administered in the diet to groups of 51 male and 51 female CDF1 mice at concentrations of 0, 0.08 and 0.16% for 76 wk. All the surviving animals were killed at wk 85 after 9 wk on the basal diet. Survival of the treated male and female mice was similar to that of the corresponding controls. The body weights were slightly lower in high- and low-dose males and in high-dose females than in the controls. All groups showed relatively high incidences of tumours of the small intestine, lung and haematopoietic organs in both sexes, of the liver and Harderian gland in males and of the uterus in females. However, there were no statistically significant differences between NA-treated and control mice of either sex in the incidences of tumours in any organs. It was therefore concluded that, under the conditions of this study, NA showed no carcinogenic potential in either male or female CDF1 mice.

Administration, Oral↗
PubMed1986

Dose-response studies on the carcinogenicity of potassium bromate in F344 rats after long-term oral administration.

Dose-response studies on the carcinogenicity of potassium bromate (KBrO3), a food additive, were undertaken to examine its effects at low doses. A total of 148 6-week-old male inbred F344 rats were divided into 7 groups. They were given KBrO3 orally in their drinking water at doses of 500, 250, 125, 60, 30, 15, and 0 ppm for 104 weeks, at the end of which time all the surviving animals were autopsied and then examined histopathologically. Shortening of the survival times and marked inhibition of body weight increase were observed in a group given 500 ppm KBrO3. The combined incidences of renal adenocarcinomas and adenomas were significantly increased in rats treated with KBrO3 at doses of 500, 250, and 125 ppm in a dose-related manner. The dose-response curve showed a sigmoid appearance. The value for the virtually safe dose (VSD), calculated by the probit model, was 0.950 ppm KBrO3 at a risk level of 10(-6). However, significant increases in the occurrence of dysplastic foci of the kidney were found in groups at doses higher than 30 ppm KBrO3. The VSD value for the dysplastic foci estimated by the gamma-multi-hit model was 0.148 X 10(-3) ppm KBrO3 at a risk level of 10(-6). In a group tested with 500 ppm KBrO3, the combined incidences for follicular adenocarcinomas and adenomas of the thyroid and for mesotheliomas of the peritoneum were shown to be significantly increased.

Adenocarcinoma↗
PubMed1985

Dose-related enhancing effect of potassium bromate on renal tumorigenesis in rats initiated with N-ethyl-N-hydroxyethyl-nitrosamine.

Dose-response studies were undertaken to investigate the enhancing activity of potassium bromate (KBrO3), a food additive, on renal tumorigenesis initiated by N-ethyl-N-hydroxyethylnitrosamine (EHEN). A total of 180 male 6-week-old F344 rats were divided into 12 groups. EHEN was given in the drinking water for the first 2 weeks at a concentration of 500 ppm for initiation of carcinogenesis. Thereafter, the rats were treated orally either with KBrO3 at a concentration of 500, 250, 125, 60, 30 or 15 ppm, or with potassium bromide (KBr) at a concentration of 1750 or 350 ppm for 24 weeks. The mean numbers of kidney dysplastic foci were significantly increased in a dose-related manner in rats treated with more than 30 ppm KBrO3. The mean number of renal cell tumors was significantly higher after treatment with KBrO3 at the highest concentration of 500 ppm. On the other hand, KBr had no effect. It was concluded that KBrO3 at doses higher than 30 ppm in the drinking water has an enhancing effect on renal tumorigenesis.

Animals↗
PubMed1984

Studies on the promoting and complete carcinogenic activities of some oxidizing chemicals in skin carcinogenesis.

Six oxidizing chemicals were tested for promoting and complete carcinogenic activities in skin carcinogenesis using female Sencar mice. In the promotion tests, the chemicals were applied twice a week for 51 weeks after initiation with dimethylbenzanthracene (DMBA). In the tests for complete carcinogenic activities, the chemicals alone were applied for 51 weeks. Benzoyl peroxide was found to be a potent promoter as reported previously. Moreover, possible complete carcinogenic action of this chemical was found in this study. Potential promoting effect was suspected in sodium chlorite. Potassium bromate, ammonium persulphate, hydrogen peroxide and sodium hypochlorite were inactive either as a promoter or a complete carcinogen.

9,10-Dimethyl-1,2-benzanthracene↗