摘要:

AbstractThe presence of kinetochore and DNA synthesis in micronuclei (MN) induced in Chinese hamster ovary (CHO) cells by clastogenic and aneuploidogenic substances such as mitomycin C (MMC) and colchicine was determined by immunofluorescence technique using CREST antikinetochore antibodies and anti‐bromodeoxyuridine (BrdUrd) antibodies. A cytofluorimetric analysis was also performed. Colchicine significantly increased micronucleated cells at least up to 96 h from the end of treatment. As expected, among colchicine‐induced micronucleated cells the majority contained at least one CREST + MN. MMC induced a significant increase in micronucleated cells up to 120 h from the end of treatment and the great majority of MN lacked kinetochore fluorescence, indicating that MMC‐induced MN were derived from acentric fragments. However, colchicine and MMC at 48 and 72 h from the end of treatment induced a significant increase of CREST— and CREST + MN, respectively, suggesting an induction of clastogenicity by colchicine and aneuploidy by MMC. The clastogenic effect of colchicine after 48 h was also confirmed by the presence of chromatid fragments in metaphase cells. A cytofluorimetric analysis indicated that, as aspected, colchicine and MMC interfere with the G2/M and S phases, respectively; however, a slight interference of colchicine with the S phase was also observed. DNA synthesis was present in MN and it was in most cases synchronous with synthesis in the main nucleus. The frequency of cells with MN in S phase observed in untreated or MMC‐treated cells is in agreement with the proportion of cells without MN showing DNA synthesis. On the contrary, the frequency of cells with MN in S phase observed in colchicine‐treated cells was significantly lower than that observed in control and MMC‐treated cells. © 1992 W

ISSN:0270-3211    

DOI:10.1002/tcm.1770120402

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

摘要:

AbstractSister‐chromatid exchange (SCE) induction and cell cycle kinetics alterations by ethyl carbamate in bone marrow of non‐gravid murine Swiss Webster, ICR/Jcl, and C57Bl/6J dams were evaluated, and data from non‐gravid females were compared with those previously reported for pregnant dams of the same strains. In addition, lung adenoma induction by ethyl carbamate in gravid Swiss Webster dams, their offspring, and in non‐pregnant Swiss Webster females was also determined. Relative cytogenetic and tumor responses in non‐gravid and gravid Swiss Webster females and their offspring were compared. In contrast to the increased sensitivity reported for gravid Swiss Webster dams versus ICR/Jcl and C57Bl/6J dams, SCE responses to 1.1, 2.2, or 3.3 mmol/kg of ethyl carbamate in non‐gravid females were approximately equivalent among strains. In Swiss Webster and C57Bl/6J (but not ICR/Jcl) strains, SCE responses in non‐gravid females at 2.2 and 3.3 were significantly lower than those of their pregnant counterparts. Tumor induction by 3.3 mmol/kg ethyl carbamate paralleled relative SCE induction with Swiss Webster dams, demonstrating a 5‐fold increase in the number of tumors relative to their offspring and a 4‐fold enhancement of tumor induction relative to their non‐pregnant counterparts. ©

ISSN:0270-3211    

DOI:10.1002/tcm.1770120403

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

摘要:

AbstractEffects of dietary bile acids and their sodium salts on the development of pepsinogen‐altered pyloric glands (PAPG) were examined in male WKY/N Crj rats initially given a single dose of 160 mg/kg body weight ofN‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) by gastric intubation. From week 3 the animals were administered basal diet containing 0.5% supplements of cholic acid (CA), deoxycholic acid (DCA), chenodeoxycholic acid (CDCA) or their sodium salts (Na‐C, Na‐DC and Na‐CDC), or 5% ascorbic acid (ASA) or its salt (Na‐AS) for 18 weeks. The concentration of DCA and Na‐DC was reduced to 0.3% from week 12. At week 20, animals were killed and the numbers of immunohistochemically‐demonstrated PAPG were determined. Values were significantly higher with Na‐C and Na‐CDC than with the corresponding parent acids, and in the Na‐C case PAPG development was greater than with MNNG alone. In addition, Na‐CDC itself induced the numbers of PAPG significantly. These results suggest that bile salts are possible intrinsic promoters of gastric carcinogenesis. They were without effect, however, on forestomac

ISSN:0270-3211    

DOI:10.1002/tcm.1770120404

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

摘要:

AbstractThe S9‐mediated mutagenesis of IQ and MeIQ inSalmonellastrain TA98 was modulated by introduction to the assay of tryptamine or tyramine. Both biogenic amines inhibited or enhanced the mutagenic response as a function of amine concentration, strain of rat used as the S9 source, and the IQ‐type mutagen tested. Enhancement of IQ mutagenesis by tryptamine (10–80 μM) was observed in the presence of S9 preparations derived from Aroclor 1254‐pretreated Fischer rats; the enhancing effect ceased at tryptamine concentrations>160 μM. When Sprague‐Dawley‐S9 or Wistar‐S9 were used for activation, the enhancement of IQ mutagenesis by tryptamine shifted to inhibition at tryptamine concentrations>40 μM, with Sprague‐Dawley‐S9, and>20μM, with Wistar‐S9. By contrast, MeIQ‐mutagenesis was enhanced by tryptamine (10 – 160μM), regardless of the rat strain used as S9 source. Tyramine was a weaker enhancer of MeIQ mutagenesis than was tryptamine and, unlike tryptamine, its inhibitory effects on IQ mutagenesis were observed only with Wistar‐S9. Tryptamine (10–80 μM) inhibited cytochromes P450IA1 and P450IA2 activities, monitored by the O‐deethylation of ethoxyresorufin and Glu‐P‐1 mutagenesis in TA98, respectively. These data suggest that the effects of biogenic amines on IQ and MeIQ bioactivation are complex. Furthermore, this study demonstrates that tryptamine and tyramine act both as enhancers (comutagens) and as inhibitors (antimutagens) of IQ and MeIQ mutagenesis, depending on the tes

ISSN:0270-3211    

DOI:10.1002/tcm.1770120405

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

ISSN:0270-3211    

DOI:10.1002/tcm.1770120401

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY