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Biomedical subjects

M Hirose

Publications and source records attributed to M Hirose.

At least 577 records · Page 32Linked to original sources
PubMed1987

Microscopic fluorometric analysis of Na-fluorescein transport in the smallest secretory unit (couplet hepatocytes) and the effects of cytochalasin B.

The uptake and secretion of sodium fluorescein by couplet hepatocytes was examined in primary culture. When sodium fluorescein was added at an early stage of primary couplet hepatocytes culture, this resulted in a rapid uptake of the dye and its subsequent accumulation in bile canaliculi. From microscopic fluorometry observations, cytochalasin B pretreatment of the couplet hepatocytes caused much more rapid uptake and secretion of the dye in bile canaliculi. The present study indicates that the cholestatic agent cytochalasin B causes choleresis at the bile canalicular level of cultured couplet hepatocytes and also indicates that a defect in canalicular secretion plays no role in the cytochalasin B-induced impairment of bile flow.

Animals↗
PubMed1986

Alpha-fetoprotein-producing pancreatoblastoma. A case report.

A case of pancreatoblastoma, arising in the tail of the pancreas with metastases to the right radius, in an 8-year-old boy is reported. The serum alpha-fetoprotein (AFP) level was over 13 times the normal value before surgery, but returned to normal after removal of the primary tumor. Furthermore, AFP was detected in tumor tissue by immunohistochemistry. This case, representing the second primary non-germ cell pancreatic neoplasm in a child producing elevated serum AFP, supports the use of serum AFP in diagnosing this lesion.

Child↗
PubMed1986

Histopathological classification of nephroblastomas in slaughtered swine.

A histological classification of 74 nephroblastomas found in slaughtered swine is reported. The tumours were classified into 4 main types; nephroblastic (29 cases); epithelial (38 cases); mesenchymal (one case), and miscellaneous (6 cases), on the basis of their histological characteristics and especially on their relative contents of epithelial and mesenchymal elements. The nephroblastic type was further divided into 3 subtypes: nephroblastic only (one case), nephroblastic predominance 13 cases) and nephroblastic equal to epithelial (15 cases). Similarly, the epithelial type was classified into two subtypes: epithelial only (one case) and epithelial predominance (37 cases). The histological features of these tumours were compared with those of human nephroblastoma. The classification of swine nephroblastomas made in this study closely resembles that of human tumours. Two examples of the nephroblastic type were metastasized but none of the other types.

Animals↗
PubMed1986

Combined effects of butylated hydroxyanisole and other antioxidants in induction of forestomach lesions in rats.

The possibility that changes in the forestomach of rats induced by butylated hydroxyanisole (BHA) are caused by inductions of free radicals and their reactions with macromolecules was examined. Groups of five male F344 rats were pretreated with 1% alpha-tocopherol, 1% ellagic acid, 1% propyl gallate, 0.25% ethoxyquin, 0.5% glutathione, 1% sodium L-ascorbate or 1% 3,3'-thiodipropionic acid for 1 week, then treated with the same antioxidant plus 1% BHA for 1 week, and then killed. Histological examination showed that BHA induced epithelial hyperplasia of the forestomach. This induction of hyperplasia was not inhibited, but increased by the antioxidants, particularly propyl gallate and ethoxyquin. Thus the induction of hyperplasia by BHA may not be related to a free radical reaction.

Animals↗
PubMed1986

Modification by antioxidants and p,p'-diaminodiphenylmethane of 7,12-dimethylbenz[a]anthracene-induced carcinogenesis of the mammary gland and ear duct in CD rats.

The effects of antioxidants on mammary gland carcinogenesis pretreated with 7,12-dimethylbenz[a]anthracene (DMBA) in female Sprague-Dawley rats were examined. The antioxidants used were butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), sodium L-ascorbate, alpha-tocopherol, ethoxyquin and p,p'-diaminodiphenylmethane (DDPM), which is an inhibitor of carcinogenesis in the liver, kidney and urinary bladder. Female Sprague-Dawley rats of 50 days old were treated with 2.5 mg/100 g body weight of DMBA, and from 1 week later were given diet supplemented with 1% BHA, 0.7% BHT, 5% sodium L-ascorbate, 1.5% alpha-tocopherol, 0.5% ethoxyquin or 0.1% DDPM for 33 weeks and then killed. The incidences of mammary tumors, carcinomas and fibroadenomas in DMBA-treated animals were reduced by diet containing BHA or ethoxyquin. Diet containing BHT or DDPM inhibited the induction of only fibroadenomas. The incidence of ear duct tumors in DMBA-treated animals was reduced by diet containing BHT, alpha-tocopherol or ethoxyquin.

9,10-Dimethyl-1,2-benzanthracene↗
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

Modifying effects of antioxidants on chemical carcinogenesis.

Studies were made on the carcinogenic activity of butylated hydroxyanisole (BHA) in rats, mice, and hamsters and the effect of the antioxidants BHA, butylated hydroxytoluene (BHT), ethoxyquin (EQ), sodium L-ascorbate (SA), ascorbic acid (AA), sodium erythorbate (SE), propyl gallate (PG), and alpha-tocopherol, on two-stage chemical carcinogenesis in rats initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 1,2-dimethylhydrazine (DMH), diethylnitrosamine (DEN), 7,12-dimethylbenz(a)anthracene (DMBA), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), N-ethyl-N-hydroxyethylnitrosamine (EHEN), or N-methylnitrosourea (MNU). BHA clearly induced squamous cell carcinomas in both the rat and hamster forestomach. The tumorigenic action of crude BHA on the forestomach is largely due to 3-tert-BHA. In two-stage chemical carcinogenesis, BHA promoted MNNG or MNU-initiated forestomach and BBN- or MNU-initiated urinary bladder carcinogenesis and inhibited DEN- or EHEN-initiated liver and DMBA-initiated mammary carcinogenesis. BHT demonstrated promotion potential for urinary bladder and MNU-initiated thyroid carcinogenesis and inhibited DMBA-initiated ear duct carcinogenesis. EQ promoted EHEN-initiated kidney carcinogenesis and inhibited DMBA-initiated mammary and EHEN-initiated liver carcinogenesis. SA promoted forestomach and urinary bladder carcinogenesis and SE likewise enhanced urinary bladder carcinogenesis. alpha-Tocopherol inhibited ear duct carcinogenesis. No effects of any of the antioxidants on glandular stomach carcinogenesis were found. The results clearly demonstrated that antioxidants have different effects (promoting or inhibitory influences) depending on the organ studied and suggest the importance of a whole body approach to their investigation.

Animals↗
PubMed1986

Disappearance of upward proliferation and persistence of downward basal cell proliferation in rat forestomach papillomas induced by butylated hydroxyanisole.

The reversibility of forestomach lesions induced in rats by butylated hydroxyanisole (BHA) was examined. F344 rats were given BHA for 24 weeks, followed by the basal diet, and their forestomach lesions at weeks 24 and 96 were compared histopathologically. Hyperplasias and papillomas showing upward proliferation were found in week 24 but not in week 96. However, downward proliferation of basal cells persisted after the discontinuation of BHA administration. This finding suggests that downward growth of basal cells is not reversible and is important in the development of BHA-induced forestomach tumors in rats.

Animals↗
PubMed1986

Sequential changes of the forestomach of F344 rats, Syrian golden hamsters, and B6C3F1 mice treated with butylated hydroxyanisole.

Butylated hydroxyanisole (BHA) was given to F344 rats, Syrian golden hamsters and B6C3F1 mice at 2 doses for up to 104 weeks. The two doses were 2.0% and 1.0% for rats and hamsters, and 1.0% and 0.5% for mice. Animals were sacrificed sequentially at 8-week intervals from week 8 to week 104, and the carcinogenic effects of BHA on the forestomach were examined histopathologically. Papillomas and carcinomas were found in rats, hamsters and mice. In rats, papillomas first appeared in week 8 in the group given the higher level of BHA and in week 56 in that given the lower level. The first carcinoma was observed in week 48 in rats given the high level, while no carcinoma was observed in rats given the lower level. In hamsters, papillomas appeared in week 8 in both BHA-treated groups, and in both groups, the incidence of papillomas was much higher than in BHA-treated rats. Squamous cell carcinomas were observed in 4 hamsters (10.0%) among those that survived more than 64 weeks on treatment with the higher level of BHA and in 4 (7.3%) among those treated with the lower level. In mice, papillomas were induced by BHA in both BHA-treated groups after more than 88 weeks. Although the incidence was not statistically significant, carcinoma was also seen in mice, suggesting that BHA may also be carcinogenic to mouse forestomach.

Animals↗
PubMed1986

Histologic and autoradiographic studies on the forestomach of hamsters treated with 2-tert-butylated hydroxyanisole, 3-tert-butylated hydroxyanisole, crude butylated hydroxyanisole, or butylated hydroxytoluene.

The inductions of hyperplasia and neoplastic lesions in the forestomach of Syrian golden hamsters by 2-tert-butylated hydroxyanisole [(2-tert-BHA) CAS: 121-00-6], 3-tert-butylated hydroxyanisole [(3-tert-BHA) CAS: 88-32-4], crude butylated hydroxyanisole [(BHA) CAS: 25013-16-5], and butylated hydroxytoluene [(BHT) CAS: 128-37-0] were compared histopathologically and autoradiographically. In hamsters fed the 2-tert-BHA diet, severe hyperplasia developed from week 4, reaching a maximum level in week 16 of 0.56 cm/10 cm basement membrane (bm), and papillomatous lesions appeared in week 16 (0.13 cm/10 cm bm). In hamsters fed 3-tert-BHA or crude BHA, severe hyperplasia developed from week 1, which reached a maximum level in week 4 of 3.63 cm/10 cm bm with 3-tert-BHA and 5.10 cm/10 with crude BHA; it then decreased. Papillomatous lesions were found in week 3 in hamsters fed 3-tert-BHA and in week 4 in hamsters fed crude BHA; they increased to maximum levels in week 16 of 0.50 cm/10 cm bm with 3-tert-BHA and 0.29 cm/10 cm bm with crude BHA. Mild hyperplasia occurred slightly more often in hamsters fed the BHT diet than in the control group. BHT induced no severe hyperplasia and papillomatous lesions. Changes in the labeling index of the forestomach epithelium paralleled the histologic changes, except in hamsters fed the BHT diet in which no significant increase in the labeling index was observed throughout the experiment. These data suggest that the tumorigenic action of crude BHA on hamster forestomach is largely due to 3-tert-BHA and that BHT does not induce forestomach tumors in hamsters.

Animals↗
PubMed1986

Dose response in butylated hydroxyanisole induction of forestomach carcinogenesis in F344 rats.

Groups of 50 6-week-old male F344 rats were given a powdered diet containing 0, 0.125, 0.25, 0.5, 1, or 2% butylated hydroxyanisole [(BHA) CAS: 25013-16-5] for 104 weeks. The highest dose--2% BHA--induced significant increase in the incidence of squamous cell carcinoma of the forestomach. Papillomas of the forestomach developed in 20 and 100% of the rats given diets containing 1 and 2% BHA, respectively. The incidence of epithelial hyperplasia of the forestomach increased with the increased BHA doses, to 100% incidence at the highest dose. Thus the incidences of proliferative and neoplastic lesions of the forestomach were dose dependent.

Animals↗