摘要:

AbstractButhionine sulfoximine (BSO) treatment significantly reduced testicular epididymal and vas deferens glutathione (GSH) levels in rats. Testicular levels of GSH were reduced by 20%, while epididymal GSH levels were reduced by more than 50%. BSO treatment correspondingly enhanced ethyl methanesulfonate (EMS)‐induced dominant lethal mutations. EMS‐induced resorption rates were doubled following BSO treatment. This effect was observed in mating wk 2 and 3 (d 8–19 following treatment), indicating effects on those germ cells which were in late testicular stages or were caput epididymal spermatozoa at the time of EMS treatment. The enhancement of the mutagenic action of EMS by BSO is restricted to the same time period (spermatid‐spermatozoa transition, early epididymal maturation) as maximum sensitivity to the clastogenic action of EMS on male germ cells. The temporal pattern of EMS alkylation of rat spermatozoa correlated with the incidence of EMS‐induced dominant lethal mutations. BSO depresses GSH in the male reproductive tract in a dose‐ and time‐dependent manner. Perturbation of GSH in the male reproductive tract appears to influence chemical‐induced germ

ISSN:0270-3211    

DOI:10.1002/tcm.1770070602

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

年代:1987

数据来源: WILEY

摘要:

AbstractV 79 hamster cells were exposed to hypotonic culture medium or to hypotonic solutions of ammonium sulfate, sodium chloride, or trishydroxymethylaminomethane. Hypotonic treatment led in all experiments to a clear increase of chromosomal aberrations. Reasons for the aberrations observed may be directly induced DNA damage such as double strand breaks or a release of DNase after lysosomal damage because of the hypotonic treatment. Other reasons involved in the aberration production may be changes of the internal pH or damage of the chromosomal proteins.

ISSN:0270-3211    

DOI:10.1002/tcm.1770070603

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

年代:1987

数据来源: WILEY

摘要:

AbstractWe present 25 new cases of blood dyscrasia, including leukemias, production defects, and thrombocytopenic purpura, generally following home termite treatment with the chlorinated hydrocarbon pesticides chlordane and heptachlor (C/H). These newly reported cases are consistent with 34 previously published case reports associating blood dyscrasias with C/H exposure. Additionally, the newly reported leukemias are consistent with epidemiologic evidence of excess risk of leukemia and other cancers in C/H‐exposed populations and with the carcinogenic action of C/H in animals. The importance of case reports in warning of the association of blood dyscrasias to C/H exposure is emphasized. Until the voluntary halt in production in July 1987, millions of homes in the United States were treated with chlordane and heptachlor for termites even though their agricultural uses were phased out in 1978, largely on the grounds of “imminent hazard” because of carcinogenicity. In view of the recognized myelotoxicity, carcinogenicity, and other chronic toxic effects of these pesticides, a national program for monitoring all homes treated is urgently needed to detect persistent contamin

ISSN:0270-3211    

DOI:10.1002/tcm.1770070604

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

年代:1987

数据来源: WILEY

摘要:

AbstractAnticonvulsant drugs are known to induce a varied pattern of malformation in both humans and in experimental rodent models. Often the clinical overlap between the pattern of defects induced by different anticonvulsant drugs is so striking that many clinicians question the role these compounds play relative to the existing maternal seizure disorder in the etiology of the observed malformations. In three inbred mouse strains exposed to phenytoin or phenobarbital in utero, the pattern of malformation differed markedly. From the types of anomalies observed, it is apparent that phenobarbital induced more malformations, while phenytoin produced a higher frequency of anomalies related to incomplete development. Thus, while there exists a certain degree of similarity between some of the minor features characteristic of each drug‐induced syndrome, there are distinct differences in pregnancy outcome in experimental animals exposed to these drugs. Given the fact that phenobarbital induces more malformations that can be traced to exposure during early organogenesis, it may be wise to consider a therapeutic strategy in which phenytoin is utilized only during organogenesis, and is then replaced with phenobarbital for the remainder of the pregnanc

ISSN:0270-3211    

DOI:10.1002/tcm.1770070605

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

年代:1987

数据来源: WILEY

摘要:

AbstractF344 male rats were irradiated once with 6 G of cesium 137 gamma rays at various times after a two‐thirds partial hepatectomy (PH) and then fed a diet containing the liver tumor promoter phenobarbital to evoke the expression of initiated hepatocytes. Yields of hepatocellular neoplasms were enumerated at 45 weeks after irradiation. Although proliferating hepatocytes in regenerating livers appeared to have increased risk of initiation by gamma rays, there was no apparent variation in risk among groups that were treated at times when hepatocytes were in different portions of the cell cycle (G1, S, G2/M). Gamma irradiation delayed the onsets of DNA synthesis and mitosis by proliferating hepatocytes by 18–20 h. The rate of rejoining of radiation‐induced DNA strand breaks was analyzed in primary cultures of hepatocytes; 98% of the strand breaks were rejoined within 30 min after irradiation. Efficient repair of certain types of radiation‐induced damage to DNA before the damaged DNA is replicated should cause a substantial reduction in the probability of induction of base‐substitution mutations. Hepatocellular islands and neoplasms that were initiated by gamma rays may be derived from proliferating hepatocytes which incurred other radiation‐induced DNA damages such as chromosomal

ISSN:0270-3211    

DOI:10.1002/tcm.1770070606

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

年代:1987

数据来源: WILEY

ISSN:0270-3211    

DOI:10.1002/tcm.1770070601

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

年代:1987

数据来源: WILEY