Biomedical subjects

H Iishi

Publications and source records attributed to H Iishi.

At least 127 records · Page 7Linked to original sources

PubMed1992

Promoting effect of ovariectomy on hepatocellular tumorigenesis induced in mice by 3'-methyl-4-dimethylaminoazobenzene.

The treatment of female C57BL/6 x DS-F1 mice with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) at 10, 12, 14, 16 and 18 days of age resulted in the development of hepatocellular adenomatous nodules after 10 months of age. Ovariectomy in these mice at 1 month of age hastened the development of adenomatous nodules, which then first appeared at 8 months of age. The incidence of adenomatous nodules in females ovariectomized at the age of 1 month was much higher than that in intact females of the same age. These results showed that the ovaries exerted a suppressive effect on the development of adenomatous nodules. To determine the time from which the ovaries exert this suppressive effect, females were ovariectomized at 4, 6, 8, and 10 months of age, and the incidences of adenomatous nodules were compared at 10 and 12 months of age. Delayed ovariectomy after 8 months of age did decrease the incidence of adenomatous nodules at 10 and 12 months of age, but ovariectomy after 4 and 6 months of age did not. When the incidence of adenomatous nodules in females ovariectomized at 10 months of age was examined over the subsequent 6 months, it became significantly higher after 14 months of age compared with that in intact females. The results show that the ovariectomy has the promoting effect on the development of adenomatous nodules in the liver induced by 3'-Me-DAB after 6 months of age.

Aging↗

PubMed1992

Enhancement of dopaminergic agonist bromocriptine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of the dopamine agonist 2-bromo-alpha-ergocryptine methanesulfonate (bromocriptine) on the incidence, number and histology of gastric cancer induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in Wistar rats. Rats were given 1 or 2 mg kg-1 body weight of bromocriptine subcutaneously every other day in depot form after 25 weeks of oral treatment with MNNG. Prolonged administration of bromocriptine at both dosages every other day resulted in a significant increase in the incidence and number of gastric cancers of the glandular stomach by week 52. Bromocriptine treatment did not influence the histological type of gastric cancer, but caused a significant increase in the labelling index of epithelial cells of the antrum. These findings indicate that the dopamine agonist bromocriptine promotes gastric carcinogenesis, and that this effect may be related to its effect in increasing proliferation of epithelial cells in the antral mucosa.

Adenocarcinoma↗

PubMed1992

Effect of treatment with cisapride alone or in combination with domperidone on gastric emptying and gastrointestinal symptoms in dyspeptic patients.

The effects on gastric emptying and gastrointestinal symptoms of treatment with cisapride alone and in combination with domperidone were investigated in 25 patients with chronic idiopathic dyspepsia. In a double-blind study, 9 patients were randomly assigned to receive cisapride 2.5 mg three times daily, and 8 patients to receive placebo. After 7 days of treatment, gastric emptying was significantly accelerated and the score of gastrointestinal symptoms was significantly reduced in patients treated with cisapride. Placebo treatment had no significant effect. A randomized, double-blind crossover study of 8 patients compared the effects of combined treatment with cisapride 2.5 mg plus domperidone 10 mg three times daily for 7 days against the effects of cisapride plus placebo. Administration of cisapride plus domperidone gave significantly higher gastric emptying and lower gastrointestinal symptoms than cisapride plus placebo.

Chronic Disease↗

PubMed1992

Effect of gamma-butyrolactone on baclofen inhibition of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of gamma-butyrolactone (GBL) on inhibition by baclofen of gastric carcinogenesis was investigated in Wistar rats. In week 52, baclofen significantly decreased the incidence of gastric cancers. Concomitant treatment with GBL significantly increased gastric acid secretion but had no influence on the inhibition by baclofen of gastric carcinogenesis. This finding suggest that GBL significantly increased the sensitivity of gamma-aminobutyric acid (GABA) receptor to GABA mimetics in gastric acid secretion but not in the inhibitory effect of gastric carcinogenesis.

4-Butyrolactone↗

PubMed1992

Attenuation by the GABA receptor agonist baclofen of experimental carcinogenesis in rat colon by azoxymethane.

The effects of the gamma-amino-n-butyric acid (GABA)A receptor agonist muscimol, and the GABAB receptor agonist baclofen, on colon carcinogenesis induced by azoxymethane in Wistar rats were tested. Administration of either muscimol or baclofen had no influence on the incidence of colon tumors at week 30. However, almost all the colon tumors that developed in rats treated with baclofen were adenomas, whereas in the control group the tumors were mainly adenocarcinomas. In contrast, administration of muscimol did not affect the histological types of the colon tumors. These findings indicate that baclofen inhibits the growth of colon tumors via the GABAB receptor.

Adenocarcinoma↗

PubMed1992

Enhancement by methionine- and leucine-enkephalin of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of the opioid receptor agonists methionine-enkephalin (Met-ENK) and leucine-enkephalin (Leu-ENK) on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in Wistar rats. After 25 weeks of oral treatment with the carcinogen, the rats received subcutaneous injections of Met-ENK (20 micrograms/kg) or Leu-ENK (20 micrograms/kg) once every 2 days. The prolonged administrations of Met-ENK and Leu-ENK significantly increased the incidence of gastric cancers in week 52. Treatments with these opioid receptor agonists significantly increased the labeling index of the antral mucosa. These findings indicate that opioids enhance gastric carcinogenesis and suggest that their effects may be related to their influence on increasing proliferation of the antral epithelial cells.

Animals↗

PubMed1992

[Evaluation of chromo-endoscopy for diagnosis of histological repair of gastric ulcer].

The chromoendoscopic features of healed gastric ulcers were investigated by the methylene blue test. Histological repair of healed ulcers was graded as either Ul3 (incompletely healed) or Ul4 (completely healed). Endoscopically, the Ul4 scar was observed as a flat granular area without any depression, and sometimes associated with redness, the Ul3 scar was observed as a distinct depression in the surrounding normal mucosal surface, and usually associated with homogenous redness. Follow-up studies of patients with Ul4 and Ul3 lesions showed that recurrence was significantly rare in patients with the Ul4 lesion than in patients with the Ul3 lesions. These findings indicate that healing of gastric ulcers should be defined endoscopically as crater disappearance. At 8 weeks after treatment with omepral, most of the ulcers were healed, but judged a as Ul3 scar.

Adenosine Triphosphatases↗

PubMed1991

Inhibition by the dopamine antagonist haloperidol of experimental carcinogenesis induced by azoxymethane in rat colon.

The effects of the dopamine agonist bromocriptine and antagonist haloperidol on the incidence and histology of colon tumors induced by azoxymethane and on the labeling index of colon mucosa were investigated in Wistar rats. Rats received weekly s.c. injections of 7.4 mg/kg of body weight azoxymethane for 10 weeks and s.c. injections of 2 mg/kg of body weight bromocriptine or 2 mg/kg of body weight haloperidol, in depot form, every other day until the end of the experiment in week 30. Administration of haloperidol resulted in a significant decrease in the incidence of colon tumors. It also caused a significant decrease in the incidence of adenocarcinomas, with 75% of the tumors being adenomas, and in the labeling index of the colon epithelial cells. In contrast, bromocriptine had no influence on the incidence or histology of colon tumors or the labeling index of the colon mucosa. These findings indicate that the dopamine antagonist haloperidol inhibits colon carcinogenesis and that this effect may be related to its effect in decreasing the proliferation of colon epithelial cells.

Adenocarcinoma↗

PubMed1991

Inhibition by retinoic acid of hepatocarcinogenesis induced by N-nitrosomorpholine and of expression of myc oncogene protein in Sprague-Dawley rats.

The effects of all-trans-retinoic acid (RA) on hepato-carcinogenesis induced by N-nitrosomorpholine (NNM) and on the expression of myc p110 proteins were investigated in male Sprague-Dawley rats. Rats received i.m. injections of RA twice a week and, from the beginning of the experiment, were given drinking water containing NNM for 8 weeks. Pre-neoplastic and neoplastic lesions staining positively for gamma-glutamyl transpeptidase (GGT), glutathione-S-transferase placental type (GST-P) or myc p110 protein were examined histochemically. At week 18, quantitative histological analysis showed that prolonged administration of RA resulted in a significant reduction in the number, size and volume of GGT-positive and GST-P-positive hepatic lesions. Administration of RA also caused a significant increase in the proportion of myc p110-negative lesions to the total pre-neoplastic lesions observed. Myc p110-negative lesions had a significantly lower mitotic index than myc p110-positive lesions. These findings indicate that RA inhibits hepatocarcinogenesis and suggest that this effect may be related to its influence in reducing the expression of myc gene proteins and its subsequent inhibition of cell proliferation in pre-neoplastic lesions.

Animals↗

PubMed1991

Roles of ovaries and testes in hepatocellular tumorigenesis induced in mice by 3'-methyl-4-dimethylaminoazobenzene.

The roles of gonads in tumorigenesis induced in mouse liver by 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) were investigated. C57BL/6 x DS-F1 mice which were 10, 12, 14, 16 and 18 days old were treated i.p. with 3'-Me-DAB. Nodular lesions induced in the liver were classified into adenomatous nodules and hepatocellular carcinomas. Adenomatous nodules were composed of a mixture of eosinophilic, basophilic, vacuolated and foamy hepatocytes in various proportions and compressed the adjacent parenchyma. These adenomatous nodules were of monoclonal origin. Carcinomas had a trabecular structure. The incidence, numbers per mouse and areas of adenomatous nodules and carcinomas in male and female mice aged 16-64 weeks were compared. Adenomatous nodules were first detected in males and females aged 24 and 52 weeks, respectively, and their incidences were much higher in males than in females of the same age. The number of adenomatous nodules per mouse and their size were also higher in males. The first carcinoma was found in a 52-week-old male, but no carcinomas were found in females even at 64 weeks of age. The effects of castration 23 days after birth on the appearance of nodular lesions in the livers of 32- to 64-week-old mice were examined. Castration of males did not affect the incidence of adenomatous nodules, but reduced the incidence of carcinomas. It also decreased the number of adenomatous nodules per mouse. Castration of females reduced the time before appearance of adenomatous nodules and increased their incidence, number per mouse, and area. A carcinoma appeared in a 64-week-old castrated female, but no similar lesion was found in intact females of the same age. These results indicate that tumorigenesis induced in mouse liver by 3'-Me-DAB is enhanced by the testes and suppressed by the ovaries.

Adenoma↗

PubMed1991

Enhancement by tyrosine methyl ester of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of tyrosine methyl ester (TME) on the incidence, number, and histological types of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in male Wistar rats. Rats were subcutaneously given TME, 512 mg/kg body weight, every other day after 20 weeks of oral treatment with MNNG. Prolonged alternate-day administration of TME caused a significant increase in the incidence and number of gastric cancers of the glandular stomach by week 52. However, it did not affect the histology of the cancers. TME also caused a significant increase in tissue norepinephrine concentrations in the antral portion of the gastric wall and in the labelling indices of the antral epithelial cells. However, TME had no influence on the serum gastrin level and antral pH. These findings indicate that TME enhances gastric carcinogenesis, and this may be related to its effects on increasing norepinephrine levels in the gastric wall and stimulating proliferation of the antral epithelial cells.

Adenocarcinoma↗

PubMed1991

Enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats fed a low-protein diet.

The effects of ad libitum feeding of synthetic, low-protein diets on the incidence and number of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in Wistar rats. Rats were fed synthetic diets of equal calorie content containing 25% casein (normal protein diet), 10% casein (low-protein diet), or 5% casein (very-low-protein diet) after treatment with N-methyl-N'-nitro-N-nitrosoguanidine p.o. for 25 weeks. Administration p.o. of a very-low-protein diet containing 5% casein resulted in a significant increase in the incidence and number of gastric cancers in experimental Week 52. However, it did not affect the histology of the cancers. The very-low-protein diet also caused a significant increase in tissue norepinephrine concentration of the antral portion of the gastric wall and in the labeling index of the antral epithelial cells. These findings indicate that a very-low-protein diet enhances gastric carcinogenesis and that this effect may be related to its effect in increasing norepinephrine in the gastric wall and stimulating proliferation of antral epithelial cells.

Animals↗

PubMed1991

Attenuating effect of the monoamine oxidase inhibitor furazolidone on the anti-carcinogenetic effect of cysteamine on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of furazolidone on inhibition by cysteamine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in inbred Wistar rats. After oral treatment with MNNG for 25 weeks, rats received cysteamine, furazolidone, or both compounds. In week 52, rats treated with cysteamine had a significantly decreased incidence of gastric cancers. Concomitant treatment with furazolidone significantly attenuated the inhibitory effect of cysteamine on gastric carcinogenesis. Administration of furazolidone alone significantly increased the number, but not the incidence, of gastric cancers. The norepinephrine concentration of the antral portion of the gastric wall and the labelling index of the antral mucosa were significantly reduced in rats treated with cysteamine, and significantly higher in rats treated with both compounds than in those treated with cysteamine alone. These findings indicate that the cysteamine-induced inhibition of gastric carcinogenesis is mediated by catecholamines.

Adenocarcinoma↗

PubMed1991

Enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine in deoxycorticosterone acetate-NaCl hypertensive rats and its inhibition by potassium chloride.

The effect of s.c. administration of deoxycorticosterone acetate (DOCA) plus p.o. treatment with NaCl solution on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and the effect of p.o. potassium supplementation on the enhanced induction of gastric carcinogenesis in DOCA-NaCl rats were investigated in Wistar rats. After 25 weeks of p.o. treatment with the carcinogen, rats received s.c. injections of DOCA (50 mg/kg) twice a week and were given 1% NaCl solution with and without 1% KCl as drinking water. In Week 52, the blood pressure, the incidence of gastric cancer, and the number of cancers per rat were significantly greater in DOCA-NaCl rats than in the untreated group. Prolonged p.o. treatment of DOCA-NaCl hypertensive rats with potassium significantly reduced their blood pressure, the incidence of gastric cancers, and their number per rat. All gastric tumors were in the glandular portions of the stomach. The norepinephrine concentration in the gastric wall and the labeling indices of gastric mucosa were significantly greater in DOCA-NaCl hypertensive rats than in the untreated group, but p.o. potassium supplementation significantly reduced the norepinephrine concentration in the gastric wall and the labeling indices of the gastric mucosa in DOCA-NaCl rats. Thus, administration of DOCA and NaCl increased the norepinephrine concentration in the gastric wall and promoted gastric carcinogenesis, and p.o. potassium supplementation decreased the norepinephrine concentration in the gastric rats. Inasmuch as the norepinephrine concentration has been used as a marker of sympathetic nervous activity, these findings suggest that the sympathetic nervous system plays an important role in gastric carcinogenesis, probably associated with cell proliferation of antral epithelial cells.

Adenocarcinoma↗

PubMed1991

Inhibition by putrescine of experimental carcinogenesis in rat colon induced by azoxymethane.

The effects of putrescine on the incidence and number of colon tumors induced by azoxymethane, and on the labelling index and the activity of ornithine decarboxylase (ODC) in the colon mucosa were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of azoxymethane and i.p. injections of 300 mumol/kg body weight of putrescine every 2 days until the end of the experiment at week 40. This prolonged treatment with putrescine significantly reduced the incidence and number of colon tumors. Administration of putrescine also significantly decreased the labelling index and the ODC activity in the colon mucosa during, but not after, treatment with the carcinogen. These last effects may be related to the action of putrescine in inhibiting the development of colonic tumors.

Adenocarcinoma↗

PubMed1991

Inhibition by neurotensin of azaserine-induced carcinogenesis in rat pancreas.

The effect of neurotensin on pancreatic carcinogenesis induced by azaserine was investigated in Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 200 micrograms/kg body weight of neurotensin in depot form every other day for 62 weeks. Carcinogen-induced pancreatic lesions were examined by histochemical techniques, and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histological analysis showed that prolonged administration of neurotensin significantly reduced the volume (as percent of parenchyma) of ATPase-positive pancreatic lesions, which are closely correlated with the ultimate development of pancreatic cancer. Histologically, pancreatic adenocarcinomas occurred at a significantly lower rate in rats treated with neurotensin than in untreated rats. Administration of neurotensin also significantly decreased the labelling indices of carcinogen-induced pancreatic lesions, but not of the surrounding acinar cells. These findings indicate that neurotensin inhibits pancreatic carcinogenesis, and that this may be related to the reduction of ATPase-positive lesions and to the inhibition of cell proliferation in neoplastic lesions of the pancreas.

Animals↗

PubMed1991

Enhancement by methionine enkephalin of colon carcinogenesis induced by azoxymethane.

The effect of the opioid receptor agonist methionine enkephalin (Met-enkephalin) and the opioid receptor antagonist naloxone on colonic carcinogenesis induced by azoxymethane was investigated in Wistar rats. Rats received ten weekly injections of 7.4 mg/kg of body weight of azoxymethane and injections of Met-enkephalin (50 micrograms/kg of body weight), naloxone (2 mg/kg of body weight), or Met-enkephalin (50 micrograms/kg of body weight) plus naloxone (2 mg/kg of body weight) once every 2 days. In wk 40, the group treated with Met-enkephalin had a significantly increased incidence of colonic tumors. A combination of Met-enkephalin and naloxone attenuated the enhancing effect by Met-enkephalin on the development of colonic tumors. Administration of naloxone alone had no influence on colonic tumorigenesis. During and after administration of the carcinogen, the bromodeoxyuridine-labeling indices of the colon mucosa and/or cancers were significantly increased in rats treated with Met-enkephalin. However, a combination of Met-enkephalin and naloxone significantly decreased the labeling indices of the colon mucosa and/or cancers. These findings indicate that Met-enkephalin enhanced colon carcinogenesis and that naloxone attenuated this enhancement. Because naloxone is an opioid receptor antagonist, these findings also indicate that the enhancing effect of Met-enkephalin on colon carcinogenesis may be mediated through opioid receptors.

Adenocarcinoma↗

PubMed1991

Enhancement by sulpiride of the inhibitory effects of cysteamine on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of sulpiride on cysteamine inhibition of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and on the BUdR labelling index of gastric mucosa were investigated in inbred Wistar rats. After 25 weeks of oral treatment with MNNG, rats received one of the following alternate-day injections: cysteamine (2 doses), cysteamine (2 doses) plus sulpiride or sulpiride. At week 52, prolonged administration of cysteamine significantly reduced the incidence of adenocarcinomas of the glandular stomach. Cysteamine at low dose had no effect on the incidence of gastric cancers, but a combination of low-dose cysteamine and sulpiride caused a significantly greater reduction in the incidence of gastric cancers. Administration of sulpiride alone had no influence on gastric carcinogenesis. The labelling index of the antral mucosa was significantly lower in rats treated with high but not low doses of cysteamine. However, a combination of low-dose cysteamine and sulpiride significantly decreased the labelling index of the antral mucosa. Our findings indicate that cysteamine suppressed gastric carcinogenesis and that sulpiride enhanced this inhibition. Because sulpiride is a dopamine antagonist, these findings also indicate that dopamine may play an important role in cysteamine inhibition of gastric carcinogenesis.

Animals↗