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Biomedical subjects

S Fukushima

Publications and source records attributed to S Fukushima.

At least 307 records · Page 17Linked to original sources
PubMed1991

[Studies on the anticomplementary activity of Jozann. Anticomplementary activity of steroid derivatives].

Methanol extracts of 53 crude drugs were tested on the anticomplementary activity. Of these, 12 samples showed the potent activity. Of these 12 samples, the extract of Jozann (Dichrome Radix) was studied on the isolation and structural elucidation of the anticomplementary constituents. As active constituents, 3 beta-hydroxystigmast-5-en-7-one was isolated and its structure was confirmed by deriving this compound from beta-sitosterol. The activity of such steroid derivatives as stigmastane, cholestane, androstane and pregnane type steroids were further studied. Of these, several kinds of steroids showed the potent activity. From these experiments, the structure and activity relationship was discussed.

Androstanes↗
PubMed1991

Colorimetric determination of fructosamine in hemolytic samples for the postmortem diagnosis of diabetes mellitus.

An analytical method of fructosamine (glycated serum protein) determination in hemolytic samples from cadavers was investigated for the postmortem diagnosis of diabetes mellitus. Fructosamine level is usually measured by the reduction of nitroblue tetrazolium (NBT) using a spectrophotometer. This assay was significantly disturbed by more than 1 g/l hemoglobin, which strongly reduced NBT by the catalytic action of the sulfhydryl and glycated groups. Glycated and total hemoglobin levels were then determined simultaneously to exclude the interferences. Total protein concentration was analyzed to eliminate dilutional effects by hemolysis. With these modifications, corrected fructosamine levels in samples containing not more than 10 g/l hemoglobin could be estimated. The assay of such hemolytic samples from 32 cadavers indicated higher fructosamine values in diabetic group than in non-diabetic subjects and the postmortem degradation of the levels as previously reported.

Adolescent↗
PubMed1991

[Phase II study of 5'-DFUR (Furtulon) capsule for bladder cancer].

A cooperative phase II study of 5'-DFUR at a daily dose of 800 to 1,200 mg was performed on 18 patients with bladder cancer. The therapeutic responses were evaluated by Koyama-Saito's criteria in 13 out of 18 patients, and 3 PR, 1 MR, 6 NC and 3 PD were obtained. Adverse reactions were observed in three out of 15 cases (20.0%). These side effects were reversible gastrointestinal symptoms such as nausea-vomiting, anorexia and diarrhea. The results suggest that 5'-DFUR is a useful drug for bladder cancer treatment.

Adenocarcinoma↗
PubMed1990

Lack of enhancing effects of fenvalerate and esfenvalerate on induction of preneoplastic glutathione S-transferase placental form positive liver cell foci in rats.

The modifying effects of fenvalerate and esfenvalerate administration on liver carcinogenesis were investigated in male F344/DuCrj rats initially treated with N-nitrosodiethylamine (DEN). Two weeks after a single dose of DEN (200 mg/kg, intraperitoneally), rats were given fenvalerate at dietary levels of 1500, 500, 150, 50 and 15 parts per million (ppm), esfenvalerate at 500 ppm, or 2-acetylamino-fluorene (2-AAF) at 200 ppm and sodium phenobarbital (PB) at 500 ppm as positive controls for 6 weeks. At week 3 following DEN administration, all animals were subjected to partial hepatectomy. Prominent neurologic signs and moderate retardation of body weight were observed in the groups given 1500 ppm fenvalerate and 500 ppm esfenvalerate, although no adverse effects on survival were evident. While statistically significant increases in relative liver weights were noted in rats given fenvalerate at doses of 1500 or 500 ppm, no toxic hepatocyte lesions were found. Neither fenvalerate nor esfenvalerate significantly increased the numbers or areas of glutathione S-transferase placental form (GST-P) positive liver cell foci observed after DEN initiation, in clear contrast to the positive controls, 2-AAF and PB. The results thus demonstrated that fenvalerate and esfenvalerate are non-toxic for rat hepatocytes and lack modifying potential for liver carcinogenesis in our medium-term bioassay system.

2-Acetylaminofluorene↗
PubMed1990

Synergism by sodium L-ascorbate but inhibition by L-ascorbic acid for sodium saccharin promotion of rat two-stage bladder carcinogenesis.

Since both sodium L-ascorbate (Na-AsA) and sodium saccharin (Na-Sac) promote two-stage bladder carcinogenesis in rats, synergism of the two chemicals was investigated with special reference to the role of urinary pH and Na+ concentration. Male F344 rats were given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine in the drinking water for 4 wk and then treated with basal diet containing 5% Na-Sac, 5% Na-AsA, 5% Na-Sac plus 5% Na-AsA, 5% L-ascorbic acid (AsA), 5% Na-Sac plus 5% AsA, or no added chemical for 32 wk. Treatment with Na-Sac or Na-AsA alone significantly increased the induction of neoplastic and preneoplastic lesions of the bladder. Na-Sac plus Na-AsA also induced these bladder lesions significantly when compared with the controls, and the number of lesions was greater than the sum of the lesions in the groups treated with Na-Sac alone or Na-AsA alone. In contrast, the induction of carcinomas and papillomas in rats treated with Na-Sac plus AsA was not significantly different from the controls. In addition Na-Sac plus Na-AsA produced an elevation of urinary pH and Na+ concentrations, although the increases were not different from those in rats fed Na-Sac or Na-AsA alone. Na-Sac plus AsA, however, did not cause elevation of urinary pH, although it increased urinary Na+ concentration. Thus, the bladder carcinogenesis promotion by Na-Sac was synergized by Na-AsA and inhibited by AsA. This modulation was associated with changes of urinary pH and Na+ concentration.

Animals↗
PubMed1990

Species differences in sodium o-phenylphenate induction of urinary bladder lesions.

The effects of sodium o-phenylphenate (Na-OPP) treatment on urinary bladder epithelium were examined in male F344 rats, B6C3F1 mice, Syrian golden hamsters and Hartley guinea pigs. Na-OPP was incorporated into diet at a dose of 2% and administered for 4, 8, 12, 24, 36 or 48 weeks. Simple and papillary or nodular (PN) hyperplasias were evident on light microscopy and pleomorphic microvilli demonstrated by scanning electron microscopy were only observed in rats, the lesions becoming more advanced with continued chemical feeding. In mice, hamsters and guinea pigs, proliferative lesions relating to Na-OPP administration were not observed. No significant differences in urinary pH, osmolality or crystal formation were apparent between the various animal species. Since carcinogenicity has been demonstrated for Na-OPP in rats but not in mice, the present findings suggest that Na-OPP might not exert urinary bladder carcinogenic potential in hamsters and guinea pigs.

Animals↗
PubMed1990

Clonal lifespans cultured in chemically defined medium and conventional bacterized medium in Paramecium octoaurelia.

The unicellular ciliate, paramecium, reproduces by binary fission, but can not continue to divide unlimitedly without sexual reproduction. We examined the clonal life span of Paramecium octaurelia stock 299 cultured in conventional bacterized medium (BM) and a chemically defined medium (DM). The cells that lived in BM divided 300 times. Although the cells in DM divided more slowly, some cells continued to divide more than 100 times. The mean life span of 90 cell lines cultured in BM was 151 +/- 49 fissions and that of 84 cell lines in DM was 68 +/- 28. When some older cells, which had been cultured in DM, were transferred to BM, most of them showed much longer life spans than those remaining in DM. The results showed that the life spans of cell clones were affected by the culture conditions.

Animals↗
PubMed1990

Carcinogenicity study of methyl hesperidin in B6C3F1 mice.

A long-term carcinogenicity study of methyl hesperidin, a compound of the vitamin P group, was carried out in B6C3F1 mice receiving dietary concentrations of 0, 1.25 or 5%. Administration was continued for 96 wk and then the mice were maintained on basal diet for an additional 8 wk. Growth retardation during the experiment with final changes in organ weights were observed in females given the 1.25% dose of methyl hesperidin and in both sexes receiving the 5.0% treatment. However, no biologically significant effects were evident with respect to mortality or clinical signs. Furthermore, treatment with methyl hesperidin did not result in any changes in haematology, clinical chemistry and urinalysis data. On histological examination, no significant alteration of non-neoplastic and neoplastic lesion incidence was observed in treated mice. The results thus demonstrated that methyl hesperidin lacked any carcinogenicity for B6C3F1 mice in the 96-wk feeding regimen used in this study.

Administration, Oral↗
PubMed1990

Bladder epithelial hyperplasia in F344 rats after intravesical instillation of the antitumor chemotherapeutic agents Adriamycin and mitomycin C.

The effects of intravesical instillation of the antineoplastic antibiotics, Adriamycin or mitomycin C, on the urinary bladder epithelium of female F344 rats were evaluated using a combined immunohistochemical and morphological approach. Four weeks treatment with Adriamycin or mitomycin C induced an increase of DNA synthesis and was associated with simple hyperplasia characterized by elevated nuclear cytoplasmic ratios, cytomegaly and pleomorphism. Under the scanning electron microscope (SEM), luminal cell surface alterations such as pleomorphic microvilli were observed. Severity of the lesions was greatest in the Adriamycin group and although treatment of the saline vehicle alone also brought about development of simple hyperplasia, this was very slight and not accompanied by cellular pleomorphism. The present results demonstrated that intravesical instillation of antineoplastic agents can cause a proliferative response and cytotoxicity after only short-term treatment and suggest that this chemotherapy could itself play a possible role in promotion of bladder carcinogenesis or cancer development.

Administration, Intravesical↗
PubMed1990

Dose response of N-butyl-N-(4-hydroxybutyl)nitrosamine on urinary bladder carcinogenesis in mutant ODS rats lacking L-ascorbic acid synthesizing ability.

With a daily intake of 250 ppm total ascorbic acid, ODS and F344 male rats were given 0.0125%, 0.025% or 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in the drinking water for 12 weeks, and additional groups received 0.05% BBN for 2, 4 or 8 weeks. The experiment was terminated after a total of 36 weeks. A greater response to urinary bladder carcinogenesis was observed in both strains with increasing dose of BBN or longer treatment period. However, the magnitude of urinary bladder carcinogenesis in ODS rats given the higher BBN concentrations and/or long periods of BBN treatment was less than in comparably treated F344 rats, but not with lower concentrations of BBN and/or shorter periods of BBN treatment.

Animals↗
PubMed1990

Immunohistochemical demonstration of carcinogen-DNA adducts in target and non-target tissues of rats given a prostate carcinogen, 3,2'-dimethyl-4-aminobiphenyl.

An immunohistochemical procedure was applied which allows accurate localization of DNA lesions within organs and tissues of rats given 3,2'-dimethyl-4-aminobiphenyl (DMAB) using polyclonal antibodies against DMAB-DNA adducts. Dose-related nuclear staining was observed in organs regardless of DMAB-carcinogenic organotropism. In the male accessory sex organs, the lateral lobe of the prostate, a non-target site, demonstrated a similar staining intensity to that found for the ventral prostate and seminal vesicle, target sites. Orchiectomy and pretreatment with ethinyl estradiol resulted in a moderate to slight decrease in binding in the accessory sex organs. No observable decrease in staining intensity was evident in most organs 168 h after the administration of DMAB. These findings suggest that DNA adduct formation itself is not necessarily sufficient for tumor induction.

Aminobiphenyl Compounds↗
PubMed1990

Different carcinogenic responses in a variety of organs, including the prostate, of five different rat strains given 3,2'-dimethyl-4-aminobiphenyl.

Tumorigenic response in the prostate of F344, ACI, Lewis, CD and Wistar rat strains to 3,2'-dimethyl-4-aminobiphenyl (DMAB) was examined in relation to development of other types of tumors. Rats of each strain aged 6 weeks were divided into two groups receiving DMAB s.c. at a dose of 50 mg/kg body wt once every other week for 10 times, with or without 1 week dietary ethynyl estradiol (EE) pretreatment. The experiment was terminated at week 60, carcinomas of the ventral prostate, all of microscopic size, being respectively found in 50, 17, 21, 15 and 0% of F344, ACI, Lewis, CD and Wistar strain animals treated with EE plus DMAB. The tumor yield correlated well with DMAB-DNA adduct formation. One invasive adenocarcinoma also developed in the periurethral part (occupying both of lateral and dorsal areas) of the prostate. The final survival rates were 46, 24, 65, 4 and 0% in F344, ACI, Lewis, CD and Wistar rats respectively. DMAB administration without EE pretreatment resulted in similar incidences of prostate tumors and mortalities. Tumors arose in greater than 14 different sites with strain dependency, lesions predominating in the skin/subcutis of ACI and F344, preputial gland of F344, urinary bladder of ACI, and mammary glands of CD rats respectively. Consideration of mortality and the relative incidence of prostate cancer and other types of tumors indicates the F344 rat strain to be the most appropriate for investigation of DMAB prostate carcinogenesis.

Aminobiphenyl Compounds↗
PubMed1990

Enhancing effects of sodium phenobarbital and N,N-dibutylnitrosamine on tumor development in a rat wide-spectrum organ carcinogenesis model.

A wide-spectrum organ carcinogenesis model for detection of cancer modifiers in various organs was assessed in F344 male rats. After sequential treatment with diethylnitrosamine, N-methylnitrosourea, and dihydroxy-di-N-propylnitrosamine, rats were fed 500 p.p.m. sodium phenobarbital (PB: carcinogen for the liver, promoter for the thyroid) in the diet or 50 p.p.m. N,N-dibutylnitrosamine (DBN: carcinogen for the upper digestive tract, liver and urinary bladder) in the drinking water. Upon histopathological investigation at experimental weeks 18 and 24, PB was found to increase significantly the incidences of hyperplasias and adenomas of the thyroid and the numbers and areas of placental glutathione S-transferase-positive foci in the liver. DBN increased the lung tumor incidences at week 18, and brought about significant increases in both numbers and areas of lung tumors per rat at week 24. Furthermore, DBN enhanced the occurrences of hyperplasias and papillomas of the esophagus as well as hyperplasia for the forestomach at both time points. In addition, significant numbers of esophageal carcinomas and lingual papillomas developed in the group given DBN after pretreatment with the three carcinogens at week 24. Assessment of lesion yield thus clearly revealed enhancement of carcinogenesis by the test chemicals in their respective target organs, indicating the advantage of the wide-spectrum organ carcinogenesis model for detection of cancer modifiers within a limited time period in multiple organs.

Animals↗