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Biomedical subjects

S Sugie

Publications and source records attributed to S Sugie.

At least 91 records · Page 5Linked to original sources
PubMed1987

Genotoxicity of a variety of nitroarenes and other nitro compounds in DNA-repair tests with rat and mouse hepatocytes.

Genotoxicity of a variety of nitroarenes and other compounds was examined in DNA-repair tests with rat or mouse hepatocytes. Out of 15 nitroarenes tested, 9 compounds, i.e., 1-nitropyrene, 1,3-dinitropyrene, 1,6-dinitropyrene, 1,8-dinitropyrene, 1-nitro-3-acetoxypyrene, 3-nitrofluoranthene, 2-nitrofluorene, 2,7-di-nitrofluorene and 5-nitroacenaphthene elicited positive response of DNA repair in the tests with rat and mouse hepatocytes. Among the positive chemicals, the DNA-repair level of the 3 dinitropyrene isomers was much higher than other nitroarenes. The results indicate that a number of nitroarenes are metabolically activated in the primary culture of rodent hepatocytes, and suggest potential carcinogenicity of 1-nitropyrene and 1-nitro-3-acetoxypyrene the carcinogenicity of which is either not clear or unknown. Of the other nitro compounds, 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide as well as 4-nitroquinoline 1-oxide were clearly genotoxic in the assays with hepatocytes of both species. However, 5-nitro-2-furaldehyde semicarbazone was negative in both assays with hepatocytes of 2 species.

Animals↗
PubMed1987

Inhibitory effect of reserpine on N-2-fluorenylacetamide-induced hepatocarcinogenesis in rats.

The effect of reserpine on N-2-fluorenylacetamide (FAA)-induced hepatocarcinogenesis was examined in female ACI rats. The incidence of hepatocellular altered foci (number/cm2) in rats of group 1 given FAA (0.02% in diet) and reserpine (subcutaneous injections of 1 microgram/g body weight, once a week) simultaneously for 10 weeks, and fed a basal diet for 17 weeks was significantly smaller than that of group 3 exposed to FAA alone for 10 weeks and given the basal diet for the subsequent 17 weeks (1.51 +/- 0.58 vs. 11.46 +/- 3.13, P less than 0.001). Similarly, the incidence of the foci of group 2 given reserpine for 16 weeks after discontinuation of FAA exposure for 10 weeks and a one-week interval of basal diet, was also significantly smaller than that of group 3 (1.51 +/- 0.62 vs. 11.46 +/- 3.13, P less than 0.001). No hepatocellular foci were seen in rats of group 4 given reserpine alone for 27 weeks and group 5 (untreated controls). These results indicate that reserpine has an inhibitory effect on FAA-initiated hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed1987

Primary signet-ring cell carcinoma of the urinary bladder.

An unusual case of the signet-ring cell carcinoma of the bladder was reported. A 62-year-old Japanese male had a three-month history of intermittent, painless and gross hematuria. He was found to have a small egg-sized bladder tumor near the right ureteral orifice. A cytologic diagnosis of signet-ring cell carcinoma was made on a bladder washing and was confirmed by cytoscopic biopsy and surgical specimens.

Adenocarcinoma, Mucinous↗
PubMed1987

Effect of in vivo exposure to the liver tumor promoters phenobarbital or DDT on the gap junctions of rat hepatocytes: a quantitative freeze-fracture analysis.

Some effects of in vivo exposure to the liver tumor promoters phenobarbital (PB) and p,p'-dichlorodiphenyltrichloroethane (DDT) on the gap junctions of hepatocytes were examined in a freeze-fracture analysis, using three groups of male ACI rats. Fifteen animals in Group 1 received a basal diet and were killed sequentially at 0, 2, 4, 6 and 8 weeks (three rats at each point) after the start of the experiment. Groups 2 (12 rats) and 3 (12 rats) were given 0.05% PB- and 0.05% DDT-containing diets respectively, and were also killed as Group 1. The frequency of hepatocyte gap junctions (per unit total membrane area) was always greater in PB-treated rats than in control rats at each killing point. In rats given DDT, the frequency of hepatocyte gap junctions was greater than in control rats at 2 and 4 weeks but was less than in control rats at 6 and 8 weeks. The average area of hepatocyte gap junctions in PB- and DDT-treated rats was significantly smaller than that in the corresponding control group (P less than 0.05-0.005). Small gap junctions within the meshwork of tight junctions were apparent only in the animals treated with PB or DDT. Promoter treatment also reduced the proportion of gap junctions per unit of hepatocyte membrane area. Furthermore, in comparison with controls, the size and distribution of gap junctional components were somewhat irregular in promoter-exposed livers. The structural changes in rat hepatocyte gap junctions observed upon in vivo exposure to PB or DDT may suggest an inhibitory effect of these agents on intercellular communication.

Animals↗
PubMed1987

Genotoxicity of a variety of nitroarenes in DNA repair tests with human hepatocytes.

The genotoxicities of 8 nitroarenes, i.e., 1-nitropyrene, 1,3-dinitropyrene, 1,6-dinitropyrene, 1,8-dinitropyrene, 2,7-dinitrofluorene, 3-nitrofluoranthene, 1-nitro-3-hydroxypyrene and 1-nitro-3-acetoxypyrene, were examined in DNA repair tests using human isolated hepatocytes. Out of the tested nitroarenes, 5 compounds, i.e., 1-nitropyrene, 1,3-dinitropyrene, 1,6-dinitropyrene, 1,8-dinitropyrene and 1-nitro-3-acetoxypyrene, clearly elicited positive responses of DNA repair. Among the chemicals which elicited positive responses, the levels of unscheduled DNA synthesis induced by the three dinitropyrene isomers were much higher than those of the other nitroarenes. Three chemicals, i.e., 2,7-dinitrofluorene, 3-nitrofluoranthene and 1-nitro-3-hydroxypyrene, elicited negative responses. The negative responses of 2,7-dinitrofluorene and 3-nitrofluoranthene, which had been positive in DNA repair tests with rodent hepatocytes, suggest some species differences between humans and rats in the metabolic activity of hepatocytes toward these agents.

Carcinogens↗
PubMed1987

Hepatocarcinogenic activities of hydroxymethyl derivatives of 4-(N,N-dimethylamino)azobenzene in ACI/N rats.

The hepatocarcinogenic potencies of three newly identified hydroxymethyl derivatives of 4-(N,N-dimethylamino)azobenzene [(DAB) CAS: 60-11-7], i.e., 2'-CH2OH-DAB, 3'-CH2OH-DAB, and 4'-CH2OH-DAB, were strictly evaluated in a long-term test (400 days) and compared to the potency of 3'-CH3-DAB. ACI/N rats, known to be less sensitive to azo dye carcinogenesis, were given one of these compounds in their diets for 120 days. The incidence of hepatocellular carcinoma in group 2 (20/20), which was given 3'-CH2OH-DAB, was much higher than that in any of the other groups: group 1 (2'-CH2OH-DAB; 4/19), group 3 (4'-CH2OH-DAB; 1/25), or group 4 (3'-CH3-DAB; 3/24). These data suggest that 3'-CH2OH-DAB is the most potent hepatocarcinogen in the series of azo dyes. Possible reasons for the potency of the chemical are discussed.

Animals↗
PubMed1986

Genotoxicity in the hepatocyte/DNA repair test and toxicity to liver mitochondria of 1-hydroxyanthraquinone and several dihydroxyanthraquinones.

1-Hydroxyanthraquinone and dihydroxyanthraquinones (alizarin, quinizarin, anthrarufin and chrysazin) were examined for genotoxicity in the hepatocyte/DNA repair test and for effects on oxidative phosphorylation in isolated rat liver mitochondria. Of the anthraquinone compounds tested, 1-hydroxyanthraquinone and 1,8-dihydroxyanthraquinone (chrysazin) induced DNA repair synthesis in rat hepatocytes, indicating their genotoxic activity. Only 1,2-dihydroxyanthraquinone (alizarin) exerted an uncoupling and inhibitory effect on mitochondrial respiration. The possible relationships of the genotoxic potencies and the uncoupling activities of these anthraquinones to their chemical structures are discussed.

Animals↗
PubMed1986

Enhancing effect of cholecystectomy on colon carcinogenesis induced by methylazoxymethanol acetate in hamsters.

The effect of cholecystectomy on colon carcinogenesis induced by methylazoxymethanol (MAM) acetate was examined in four groups of Syrian golden hamsters. For the sexes combined, the incidences of total large intestinal neoplasms and adenomas in Group 1, which received cholecystectomy and a single intravenous injection of MAM acetate (20 mg/kg body weight), were significantly higher than those of hamsters in Group 2, which were given MAM acetate alone. The combined multiplicities of total large intestinal neoplasms from male and female hamsters, and the multiplicities of those in females of Group 1 were also significantly higher than those in animals in Group 2, respectively. No intestinal tumors were observed in hamsters in Group 3 (cholecystectomy alone) or Group 4 (untreated control). These results indicate an enhancing effect of cholecystectomy on MAM acetate-induced large intestinal carcinogenesis in hamsters.

Adenocarcinoma↗
PubMed1986

Genotoxic effects of a variety of sterigmatocystin-related compounds in the hepatocyte/DNA-repair test and the Salmonella microsome assay.

The genotoxicity and mutagenicity of 11 fungal metabolites structurally related to sterigmatocystin were examined in the hepatocyte primary culture/DNA-repair test and the Salmonella microsome assay. 10 out of the mycotoxins, i.e. dihydrosterigmatocystin, 5-methoxysterigmatocystin, 5-methoxydihydrosterigmatocystin, 5,6-dimethoxysterigmatocystin, 5,6-dimethoxydihydrosterigmatocystin, sterigmatin, O-methylsterigmatocystin and O-acetylsterigmatocystin showed a positive response for DNA repair, suggesting their carcinogenic potency. 5-Methoxysterigmatocystin, 5,6-dimethoxysterigmatocystin demethylsterigmatocystin and O-acetylsterigmatocystin were mutagenic in TA100 of the bacterial mutagenicity assay with liver S9.

Acetylation↗
PubMed1986

Carcinogenicity of betel quid. III. Enhancement of 4-nitroquinoline-1-oxide- and N-2-fluorenylacetamide-induced carcinogenesis in rats by subsequent administration of betel nut.

The effect of betel nut on chemical carcinogenesis in the upper digestive tract and liver was examined in two different experimental models with ACI rats. The incidences of neoplasms and preneoplastic lesions of the tongue in animals given 5 ppm 4-nitroquinoline-1-oxide (4-NQO; CAS: 56-57-5) in the drinking water for 16 weeks and followed by 20% betel nut in the diet for 40 weeks were significantly higher than those in animals given 4-NQO alone. No enhancing effect from betel nut on the incidences of neoplastic and preneoplastic lesions in the upper digestive tract was found in animals administered 4-NQO for 12 weeks. The number of altered liver cell foci in rats given 200 ppm N-2-fluorenylacetamide (FAA; CAS: 53-96-3) in the diet for 8 weeks and followed by the betel nut diet for 16 weeks was significantly greater than that in animals fed the FAA diet alone. These results indicate enhancing effects of dietary administration of betel nut on oral carcinogenesis by 4-NQO and hepatocarcinogenesis initiated by FAA.

2-Acetylaminofluorene↗
PubMed1986

Genotoxicity of a variety of azobenzene and aminoazobenzene compounds in the hepatocyte/DNA repair test and the Salmonella/mutagenicity test.

Genotoxicity of 39 azo dye compounds of azobenzenes, aminoazobenzenes, and diaminoazobenzenes was examined in the hepatocyte primary culture/DNA repair test. Azobenzene (AzB) and 3,3'- or 4,4'-substituted azobenzenes such as (CH3)2AzB, (CH2OH)2AzB, (CH2OCOCH3)2AzB, and (CH2Cl)2AzB did not generate DNA repair, indicating lack of genotoxicity of these compounds. In contrast, all of 24 aminoazobenzenes, including those of unknown carcinogenicity, i.e., 3'-methyl-4-aminoazobenzene, 3'-CH2OH-aminoazobenzene, 3'-hydroxymethyl-N-methyl-4-aminoazobenzene, 3'-COOH-methylaminoazobenzene, 4'-formyl-N,N-dimethyl-4-aminoazobenzene, 3'-CH2Cl-dimethylaminoazobenzene, 4'-CH2Cl-dimethylaminoazobenzene, and 2'-, 3'-, or 4'-CH2OCOCH3-dimethylaminoazobenzene, elicited DNA repair synthesis. A positive DNA repair response was obtained for the 3 of 6 tested diaminoazobenzenes, i.e., N'-acetyl-N'-methyl-4-amino-dimethylaminoazobenzene, N'-acetyl-N'-methyl-4-amino-methylaminoazobenzene, and N'-acetyl-N'-methyl-4-amino-N-acetyl-methylaminoazobenzene, which are known to be carcinogenic. These results indicate that the amino group is functional for the expression of genotoxicity of azobenzene compounds. Twenty-one azobenzenes of these 3 classes were also examined for their mutagenicity in the Salmonella/mutagenicity assay. These results were almost identical with those of the DNA repair test except for several azo dyes such as AzB and 4,4'-(CH2Oacetyl)2AzB of the azobenzenes and N'-acetyl-4-amino-dimethylaminoazobenzene and N'-acetyl-N-methyl-4-amino-N-acetyl methylaminoazobenzene of the diaminoazobenzenes.

Animals↗
PubMed1986

Inhibitory effects of polyprenoic acid (E-5166) on N-2-fluorenylacetamide-initiated hepatocarcinogenesis in rats.

The effects of the newly synthesized polyprenoic acid, 3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid (E-5166) on N-2-fluorenylacetamide (FAA)-initiated hepatocarcinogenesis were examined in 6 groups of male ACI rats. The numbers of altered hepatocellular foci in rats of group 1 given a basal diet containing 0.02% FAA for 13 weeks and in rats of group 2 which received E-5166 by gavage (40 mg/kg, 3 times/week) at the same time as receiving the FAA diet were almost the same, indicating that E-5166 had no effect at the stage of carcinogen exposure. However, the number of foci in group 4, in which rats were given the basal diet and E-5166 after the termination of the carcinogen exposure, and were sacrificed 16 weeks later, was significantly smaller than that in group 3 maintained on the basal diet alone (P less than 0.05). The results suggests some anticarcinogenic activity of E-5166, possibly involving the phenotypic expression of the preneoplastic foci. Furthermore, the number of altered foci in rats of group 6 (given the liver-tumor promoter phenobarbital with E-5166 for 16 weeks after the administration of carcinogen) was also significantly smaller than that in rats of group 5, which received the promoter (P less than 0.05). The incidence of neoplastic nodules of the liver in group 6 at the end of the experiment was also lower than in group 5 (P less than 0.0014). These results suggest an antipromoting effect of the polyprenoic acid E-5166 on rat chemical hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed1986

Carcinogenicity of chrysazin in large intestine and liver of mice.

The carcinogenicity of chrysazin (1,8-dihydroxy-9,10-anthracenedione) was examined by dietary administration to C3H/HeN mice. All of the effective mice (17) which were given 0.2% chrysazin diet and which survived more than 500 days developed adenomatous hyperplasia with cystic glands of the cecum. Similar lesions were also seen in the colon of mice in this group. These intestinal lesions were not obtained in any effective mouse (19) of the control group. The incidence of hepatocellular carcinoma of mice given chrysazin (4/17) was significantly higher than that of the controls (0/19). These results indicate that chrysazin is carcinogenic in mice as well as in rats. Some mechanistic aspects of the causation of these intestinal lesions and liver neoplasms are also discussed.

Animals↗
PubMed1986

[Evaluation of prostate aspiration biopsy for cytological detection of prostate cancer].

The aspiration biopsy of the prostate for cytological detection was evaluated in 143 patients with clinically suspected prostate cancer and compared with the pathological diagnosis by needle biopsy performed simultaneously. Histopathological evaluation was possible in 136 cases. Sufficient cells for cytological diagnosis were obtained in 92.3% of pathologically diagnosed cases. Only 3 specimens for cytology (4.3%) of the prostate cancer before treatment were insufficient for cytology. Compared with pathological diagnosis by needle biopsy, false positive and negative rates were observed in 4.8% and 25.0% respectively. The accuracy rate of cytological diagnosis was higher the higher the degree of anaplasia in the pathological findings. In 20 clinically well-controlled patients the cytological results were negative in all of the well differentiated adenocarcinomas, whereas positive in poorly differentiated ones without exception. The cytological findings were still positive in all of the 4 cases with progressive cancer in spite of the anticancer therapy. Besides these results, because of no complication in the 182 aspiration biopsies, this may be a useful method for detection of prostate cancer, especially for screening of the cancer and judgment of efficacy during treatment.

Biopsy, Needle↗
PubMed1985

Cytotoxicity and genotoxicity of xenoclauxin and desacetyl duclauxin from Penicillium duclauxii (Delacroix).

The duclauxin derivatives xenoclauxin and desacetylduclauxin were examined for their effects on the growth of L-1210 murine leukemia cells, on the induction of DNA repair in the rat and mouse hepatocyte primary culture (HPC/DNA repair test), and on oxidative phosphorylation in mitochondria from rat livers in comparison to duclauxin. Both derivatives inhibited the growth of L-1210 culture cells as strongly as duclauxin. Duclauxin derivatives were negative in the HPC/DNA repair test. Xenoclauxin exhibited a potent uncoupling effect accompanying a marked depression of state 3 respiration of mitochondria in a similar fashion to that of duclauxin. Desacetylduclauxin significantly inhibited the state 3 respiration without causing uncoupling of oxidative phosphorylation in mitochondria. These results strongly suggest that xenoclauxin and desacetylduclauxin from Penicillium duclauxii are not genotoxic but are cytotoxic mainly due to their potent inhibition of ATP synthesis in mitochondria.

Animals↗
PubMed1985

Genotoxicity of carcinogenic N-nitrosopropylamine derivatives in the hepatocyte primary culture/DNA-repair test.

The genotoxicity of N-nitrosodipropylamine, 8 of its oxidized derivatives and N-nitroso-2,6-dimethylmorpholine was examined in the hepatocyte primary culture (HPC)/DNA repair test. Nine N-nitrosamines which are known to be carcinogenic and mutagenic were clearly positive in the HPC/DNA-repair test. N-Nitroso(2,3-dihydroxypropyl) (2-hydroxypropyl)amine did not elicit DNA repair, but showed a borderline mutagenic response in the Salmonella/microsome test. Thus, the HPC/DNA-repair test displays a comparable capacity to the bacterial mutagenesis test for detecting the genotoxic effects of this class of carcinogens.

Animals↗
PubMed1985

Genotoxicity of fungal metabolites related to aflatoxin B1 biosynthesis.

The genotoxicity of several anthraquinone compounds metabolically related to aflatoxin B1 was examined by means of the hepatocyte primary culture (HPC)/DNA repair test and the Salmonella microsome mutagenesis test, and compared to versicolorins A and B which are potent mutagenic and genotoxic intermediates of the aflatoxin biosynthetic pathway. 6,8-O-Dimethyl-versicolorins A, B and 6-deoxyversicolorin A were found to be strongly mutagenic and genotoxic. Genotoxicity of versicolorin A and 6,8-O-dimethylversicolorin A was stronger than that of versicolorin B and 6,8-O-dimethylversicolorin B, respectively, in the HPC/DNA repair test. Nidurufin and norsolorinic acid, which do not possess a bisfuran ring, exhibited questionable activities for mutagenicity and no genotoxicity. It is suspected that 6,8-O-dimethylversicolorins A, B and 6-deoxyversicolorin A as well as versicolorins A and B are genotoxic carcinogens.

Aflatoxin B1↗