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Comparative study of micronucleus assay and chromosomal aberration analysis in V79 cells exposed to ethylene oxide |
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Teratogenesis, Carcinogenesis, and Mutagenesis,
Volume 11,
Issue 5,
1991,
Page 227-233
Bao‐Zhen Zhong,
Zu‐Wei Gu,
Wen‐Zong Whong,
William E. Wallace,
Tong‐Man Ong,
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摘要:
AbstractMicronucleus formation and chromosomal aberration (CA) in V79 cells were compared for their sensitivity in response to ethylene oxide (EtO) treatment. The results indicate that EtO exposure for 30 min induced CAs in V79 cells at the concentration of 3,500 ppm or higher. A statistically significant difference (P<0.01) was found between treated and control groups at all concentrations tested based on percent aberrant cells. The increase was dose‐dependent with a correlation coefficient of 0.88. The aberrations found include chromatid and isochromatid breaks, fragments, minutes, and exchanges. Results of the micronucleus assay both in mononucleated and binucleated cells showed a slight but not statistically significant increase in micronuclei with doses between 457 to 4115 ppm. At the highest concentration tested (12344 ppm) EtO caused a significant increase in the micronucleus frequency (P<0.05). © 1992 Wiley‐Liss,
ISSN:0270-3211
DOI:10.1002/tcm.1770110502
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1991
数据来源: WILEY
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2. |
Heat shock proteins in human and mouse embryonic cells after exposure to heat shock or teratogenic agents |
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Teratogenesis, Carcinogenesis, and Mutagenesis,
Volume 11,
Issue 5,
1991,
Page 235-244
Ken‐Ichi Honda,
Takumi Hatayama,
Ken‐Ichi Takahashi,
Munehiko Yukioka,
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摘要:
AbstractIn human chorionic villus tissue at the 10–17th week of a normal pregnancy, heat shock proteins (hsp70, hsp73, hsp85, and hsp105) were induced in vitro by a heat shock or by exposure to sodium arsenite or cadmium chloride. In dispersed cells of the whole mouse embryo on the 11th day of development, heat shock proteins (hsp73 and hsp105) were induced by a heat shock or by exposure to sodium arsenite, but not by exposure to cadmium chloride. After a maternal hyperthermia or an intraperitoneal injection of sodium arsenite or cadmium chloride into a pregnant mouse, heat shock proteins accumulated in the embryo on the 9th day of development, especially in the neuroepithelial tissue. The significance of heat shock proteins in the embryo is discussed. © 1992 Wiley‐Liss,
ISSN:0270-3211
DOI:10.1002/tcm.1770110503
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1991
数据来源: WILEY
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3. |
Dose response study of N‐nitrosodiethanolamine initiation of rat hepatocarcinogenesis |
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Teratogenesis, Carcinogenesis, and Mutagenesis,
Volume 11,
Issue 5,
1991,
Page 245-250
Kumiko Ogawa,
Ryohei Hasegawa,
Shigetsugu Wada,
Shuji Yamaguchi,
Nobuyuki Ito,
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摘要:
AbstractInitiating activity of N‐nitrosodiethanolamine (NDELA) for rat liver carcinogenesis was investigated using an 8‐weeks bioassay system. Male F344 rats were initially treated with a single intraperitoneal injection of NDELA at one of five dose levels: 1,600, 800, 400, 200, or 100 mg/kg. Two weeks later, the rats were placed on 0.02% 2‐acetylaminofluorene (2‐AAF) or 0.05% phenobarbital (PB) containing diet for 6 weeks. All animals were subjected to 2/3 partial hepatectomy 4 weeks after the NDELA treatment, and killed at the end of the eighth week. NDELA itself exerted low toxicity in terms of body weight gain. Clear dose‐dependent initiating activity of NDELA was observed in terms of development of glutathione S‐transferase placental form (GST‐P) positive liver cell foci, this being more apparent with PB promotion than with 2‐AAF where the enhancing regimen itself caused multiple lesion development. Initiating potential of NDELA, however, was much lower than that observed for diethylnitrosamine in our previous work. © 1992
ISSN:0270-3211
DOI:10.1002/tcm.1770110504
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1991
数据来源: WILEY
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4. |
Induction of micronuclei in rat bone marrow by four model compounds |
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Teratogenesis, Carcinogenesis, and Mutagenesis,
Volume 11,
Issue 5,
1991,
Page 251-258
Xiao‐Chun Shi,
Gopala Krishna,
Tong‐Man Ong,
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摘要:
AbstractStudies have been performed to determine the dose and sampling time responses of micronuclei after Sprague‐Dawley rats were treated wth triethylenemelamine, mitomycin C. dimethylbenzanthracene, and vincristine by a single intraperitoneal injection. Three doses were tested for each compound. Animals were sacrificed 24, 48, and 72 h after chemical treatment. Slides prepared from the bone marrow were stained with May‐Gruenwald and Giemsa stains. The number of micronucleated polychromatic erythrocytes among 2,000 polychromatic erythrocytes (PCEs) and the ratio of PCEs to normochromatic erythrocytes were determined for each animal. The results show that all four compounds cause micronucleus formation in rat bone marrow. The peak response sampling time, either 24 or 48 h posttreatment, is dependent on the chemical as well as the dose. In all cases, however, an increase in the micronucleated PCEs was detected 24 h after chemical treatment. These results seem to indicate that two sampling times, 24 and 48 h, may be adequate for the micronucleus assay using rat bone marrow cells. © 1992 Wiley‐Lis
ISSN:0270-3211
DOI:10.1002/tcm.1770110505
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1991
数据来源: WILEY
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5. |
Hyperploid cells in the limb buds of rats and 5‐azacytidine‐induced digital deformities |
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Teratogenesis, Carcinogenesis, and Mutagenesis,
Volume 11,
Issue 5,
1991,
Page 259-265
Akihiro Kurishita,
Toshio Ihara,
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摘要:
AbstractTo clarify the mechanism underlying the digital teratogenesis of 5‐azacytidine (5‐AC), the DNA contents of mesenchymal cells were examined in the limb buds of the rat by microspectrophotometry. 5‐AC induced hyperploid cells: 2.4% at 18 h after injection and 3.2% at 24 h. No hyperploid cells were noted 30 h after the treatment. Because posttreatment caffeine suppressed 5‐AC‐induced digital defects, the actions of caffeine on 5‐AC‐induced hyperploid cells were further studied; no hyperploid cells were detected at any sampling point. Caffeine suppressed hyperploid cells as well as digital defects. These results suggest that the causative factors of digital defects by 5‐AC may involve hyperploid cells. However, in that there were too few hyperploid cells to cause the defects, further studies are required to clarify the nature of the action of 5‐AC. © 19
ISSN:0270-3211
DOI:10.1002/tcm.1770110506
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1991
数据来源: WILEY
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6. |
Ontogeny of peroxidase activity in epithelium and eosinophils of the mouse uterus |
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Teratogenesis, Carcinogenesis, and Mutagenesis,
Volume 11,
Issue 5,
1991,
Page 267-278
Retha R. Newbold,
Peter H. Jellinck,
Manfred Metzler,
John A. McLachlan,
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摘要:
AbstractOutbred CD‐1 mice treated for 1 or 4 days with 1 mg/kg of diethylstilbestrol (DES) at various ages after birth were examined for histochemical localization of peroxidase in the uterine epithelium. Peroxidase activity in uterine extracts was also measured by a radiometric assay and the conversion of [3H]DES to [3H]Z,Z‐dienestrol (Z,Z‐DIES). While no peroxidase activity was detected by a histochemical method in uterine epithelium from untreated 5‐day old mice, the enzyme was apparent in mice treated for 4 days with DES; uterine eosinophils were absent at this age. By day 9, DES‐induced staining for peroxidase in uterine epithelial cells and the number of uterine eosinophils had increased significantly. In addition, at this age, the biochemical assays for uterine peroxidase were sensitive enough to show that DES is converted to Z,Z‐DIES and that [3H]estradiol gives rise to3H2O and water‐soluble radioactive metabolites. The peroxidase response to DES, determined by both histochemical and biochemical methods, increased with the age of the immature mice. These data indicate that the neonatal uterus, although deficient in eosinophils, demonstrates a peroxidase response to estrogen and that this response is localized primarily in the luminal epithelium. The role of this DES‐induced peroxidase activity in converting DES to activated metabolites that may cause cell damage is discussed. © 1992
ISSN:0270-3211
DOI:10.1002/tcm.1770110507
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1991
数据来源: WILEY
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7. |
Masthead |
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Teratogenesis, Carcinogenesis, and Mutagenesis,
Volume 11,
Issue 5,
1991,
Page -
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PDF (101KB)
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ISSN:0270-3211
DOI:10.1002/tcm.1770110501
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1991
数据来源: WILEY
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