Teratogenesis, carcinogenesis, and mutagenesis最新文献

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Evaluation of EMS-induced DNA damage in the single cell gel electrophoresis (Comet) assay and with flow cytometric analysis of micronuclei. 单细胞凝胶电泳(Comet)试验和微核流式细胞术分析评价ems诱导的DNA损伤。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2003-01-01 DOI: 10.1002/tcm.10081
Elizabeth D Wagner, Diana Anderson, Alok Dhawan, A Lane Rayburn, Michael J Plewa
{"title":"Evaluation of EMS-induced DNA damage in the single cell gel electrophoresis (Comet) assay and with flow cytometric analysis of micronuclei.","authors":"Elizabeth D Wagner,&nbsp;Diana Anderson,&nbsp;Alok Dhawan,&nbsp;A Lane Rayburn,&nbsp;Michael J Plewa","doi":"10.1002/tcm.10081","DOIUrl":"https://doi.org/10.1002/tcm.10081","url":null,"abstract":"<p><p>Toxic agents in the environment pose serious threats to ecosystems and to the public health. The single cell gel electrophoresis (SCGE) or Comet assay quantitatively measures genomic damage as DNA strand breaks. The micronucleus (MCN) test is an established assay that measures chromosomal damage. Micronuclei are formed from chromosome fragments or from whole chromosomes that have not undergone mitosis properly. This test is usually conducted microscopically. However, micronuclei can also be analyzed using flow cytometry. Chinese hamster ovary (CHO) cells were exposed to ethylmethanesulfonate (EMS), for 4 h in a total volume of 25 microl. These cells were immediately analyzed for genomic DNA damage by SCGE. In concurrent parallel experiments, CHO cells were treated with EMS in 6-well plates for 4 h, the cells were washed and fresh medium was added. The cells were allowed to grow for 45 to 48 h to express micronuclei. The data demonstrated that both DNA strand breaks and micronuclei were induced in a significant and concentration-dependent manner. There was a significant and high correlation (r = 0.91; P < or = 0.001) between the acute induction of DNA strand breaks and the subsequent generation of micronuclei. These data indicate that using molecular and computer technologies, the genotoxic impact of toxic and environmental agents can be rapidly and comprehensively evaluated in mammalian cell systems.</p>","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"Suppl 2 ","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/tcm.10081","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24138151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 26
Determination of allelic deletion of multiple endocrine neoplasm type 1 (MEN1) gene in acute myeloid leukemia (AML) by application of FISH-TSA technique. 应用FISH-TSA技术检测急性髓性白血病(AML)多发内分泌肿瘤1型(MEN1)基因等位基因缺失。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/tcm.10033
Hasan Acar, Murat Kaynak, Tahsin Yakut, Fahri Uçar, Unal Egeli
{"title":"Determination of allelic deletion of multiple endocrine neoplasm type 1 (MEN1) gene in acute myeloid leukemia (AML) by application of FISH-TSA technique.","authors":"Hasan Acar,&nbsp;Murat Kaynak,&nbsp;Tahsin Yakut,&nbsp;Fahri Uçar,&nbsp;Unal Egeli","doi":"10.1002/tcm.10033","DOIUrl":"https://doi.org/10.1002/tcm.10033","url":null,"abstract":"<p><p>We have used the single and dual color fluorescence in situ hybridization (FISH) technique combined with a new detection system, tyramide signal amplification (TSA), by using the multiple endocrine neoplasm type 1 (MEN1) gene and chromosome 11 specific alpha satellite DNA probes for the study of the allelic deletion of the MEN1 gene. The MEN1 gene is a new tumor suppressor gene and has been recently cloned on chromosome 11q13. FISH combined with the TSA detection system was performed on bone marrow interphase nuclei of 22 patients with acute myeloid leukemia (AML). The FISH-TSA analysis revealed the mono allelic deletion of the MEN1 gene in 4 out of 22 patients (18.18%), 2 of 9 AML-M2 patients (22.2%), 1 of 6 AML-M4 patients (16.6%), and 1 of 4 AML-M5 patients (25.0%). Our study indicates that allelic deletion of the MEN1 gene is not a major cause or a primary event in tumorigenesis of AML, although the long arm (q13 region) of chromosome 11 involves a chromosomal rearrangement in AML.</p>","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"22 5","pages":"369-75"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/tcm.10033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21972533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Genetic polymorphisms in the cytochrome P450 1A1, glutathione S-transferase M1 and T1, and susceptibility to colon cancer. 细胞色素P450 1A1、谷胱甘肽s -转移酶M1和T1的遗传多态性与结肠癌易感性。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/tcm.10035
Zheng Ye, James M Parry
{"title":"Genetic polymorphisms in the cytochrome P450 1A1, glutathione S-transferase M1 and T1, and susceptibility to colon cancer.","authors":"Zheng Ye,&nbsp;James M Parry","doi":"10.1002/tcm.10035","DOIUrl":"https://doi.org/10.1002/tcm.10035","url":null,"abstract":"<p><p>Several polymorphic cytochrome P-450 and glutathione S-transferase (GST) enzymes are involved in the activation and detoxification of many potential carcinogens and may therefore be important in susceptibility to cancer induction. CYP1A1 MspI, GSTM1, and GSTT1 are polymorphic enzymes and some alleles have been correlated with an increased risk of developing some cancers. In the present study, we examined possible associations between genetic polymorphisms of CYP1A1 MspI, GSTM1, and GSTT1 and colon cancer in a United Kingdom population. An excess of CYP1A1 MspI, and GSTM1 null genotypes was observed amongst colon cancer patients, although this did not reach the level of statistical significance. We found no significant increase in the risk of colon cancer for either CYP1A1 MspI (OR = 1.39; 95%CI: 0.46-4.21) or GSTM1 null (OR = 1.41; 95%CI: 0.76-3.01) genotypes. Individuals with GSTT1 null genotype had no association with colon cancer (OR = 0.42; 95%CI: 0.09-2.02). No significant association was observed in the site of colon cancer (proximal vs. distal). This study suggests that the polymorphisms of CYP1A1 MspI, GSTM1, and GSTT1 are not associated with a significant risk of developing colon cancer in a United Kingdom population.</p>","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"22 5","pages":"385-92"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/tcm.10035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21972535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 42
Chromosomal fragile sites and relationship between genetic predisposition to small cell lung cancer. 染色体脆性位点与小细胞肺癌遗传易感性的关系。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/TCM.1036
M. Karadağ, B. Tunca, G. Cecener, U. Egeli, N. Ozyardimci, E. Ege, O. Gözü
{"title":"Chromosomal fragile sites and relationship between genetic predisposition to small cell lung cancer.","authors":"M. Karadağ, B. Tunca, G. Cecener, U. Egeli, N. Ozyardimci, E. Ege, O. Gözü","doi":"10.1002/TCM.1036","DOIUrl":"https://doi.org/10.1002/TCM.1036","url":null,"abstract":"Fragile sites are non-staining gaps and breaks on mammalian chromosomes. Several investigators have pointed out that these sites may act as factors that predispose to specific chromosomal rearrangements that are present in some cancer cases. The expression of common fragile sites induced by aphidicolin (Apc) was evaluated on prometaphase chromosomes obtained from the peripheral blood lymphocytes of 15 patients with lung cancer, 20 of their clinically healthy family members, and 20 age-matched normal controls. As a result of cytogenetic evaluation carried out by the High Resolution Banding (HRB) technique, 1q21, 2q33, 3p14, 7q32, 13q13, 16q23, 17q21, and 22q12 are defined as fragile sites in patients and relatives. The rate of total fragile sites and 2q33, 3p14, and 16q23 are statistically significant in both patients and relatives when compared with the control group. Therefore, our results showed that common fragile sites might be unstable factors in the human genome and they can be used as suitable markers for genetic predisposition to lung cancer.","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"162 1","pages":"31-40"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84997934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
Diabetes teratogenicity in mice is accompanied with distorted expression of TGF-beta2 in the uterus. 小鼠的糖尿病致畸性伴随着子宫中tgf - β 2的扭曲表达。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/TCM.1039
A. Fein, N. Magid, S. Savion, H. Orenstein, J. Shepshelovich, A. Ornoy, A. Torchinsky, V. Toder
{"title":"Diabetes teratogenicity in mice is accompanied with distorted expression of TGF-beta2 in the uterus.","authors":"A. Fein, N. Magid, S. Savion, H. Orenstein, J. Shepshelovich, A. Ornoy, A. Torchinsky, V. Toder","doi":"10.1002/TCM.1039","DOIUrl":"https://doi.org/10.1002/TCM.1039","url":null,"abstract":"Early embryonic deaths as well as malformed newborns are among complications of the diabetic pregnancy. Cytokines and growth factors operating in the embryonic vicinity are found to be among factors that determine the sensitivity of embryos to external and internal detrimental stimuli, including diabetes. Transforming Growth Factor-beta2 (TGF-beta2) has been shown to be essential for embryonic development and survival. In the present work, we evaluated the pattern of TGF-beta2 expression in the uterus of streptozotocin-induced diabetic mice, demonstrating a decreased reproductive performance and elevated percentage of litters with severely malformed fetuses. Since stimulation of the maternal immune system was found to increase the resistance of mouse embryos to the teratogenic effect of diabetes, the effect of immunopotentiation on the expression of the cytokine was also investigated. TGF-beta2 expression was studied at the mRNA level by using the in situ hybridization technique and at the protein level by using the immunohistochemical analysis. A clear decrease in TGF-beta2 mRNA expression in the uterus of diabetic mice was observed at examined time points: days 1, 5, and 9 of pregnancy. Also, an evident reduction in TGF-beta2, the protein expression in the uterus of diabetic mice, was demonstrated at these time points. Maternal immunopotentiation that improved the reproductive performance of diabetic mice and reduced the number of the litters with malformed fetuses was also accompanied by a clear increase in the level of TGF-beta2 mRNA expression in the pregnant uteri. The above results clearly demonstrate that the embryotoxic effect of diabetes is accompanied by an alteration of TGF-beta2 expression. Immunopotentiation that was shown to improve the reproductive performance of the diabetic mice was accompanied by a partial normalization of TGF-beta2 expression in embryonic vicinity.","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"84 1","pages":"59-71"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88347062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 23
Incision of AP sites in lung cancer patients: a pilot study. 肺癌患者AP部位切开:一项初步研究。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/TCM.10018
O. Rossi, R. Filiberti, M. Neri, Stefano Biggi, Livia Satragno, R. Puntoni, G. Fròsina
{"title":"Incision of AP sites in lung cancer patients: a pilot study.","authors":"O. Rossi, R. Filiberti, M. Neri, Stefano Biggi, Livia Satragno, R. Puntoni, G. Fròsina","doi":"10.1002/TCM.10018","DOIUrl":"https://doi.org/10.1002/TCM.10018","url":null,"abstract":"DNA base excision repair (BER) removes frequent DNA lesions of either endogenous or exogenous origin. Some indications point to BER defects in lung cancer patients. We have investigated the ability of ten lung cancer patients to repair natural AP sites, the most frequent genetic lesion, using an in vitro assay in which peripheral blood lymphocytes (PBL) extracts incise randomly depurinated plasmid DNA. The median value of repair activity in patients was lower than that of matched controls but the difference did not reach significance. Unlike other BER enzymatic steps, marked defects in incision of AP sites may not be associated with lung carcinogenesis.","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"24 1","pages":"251-6"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84755878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Effect of disulfiram on the genotoxic potential of acetaldehyde in mouse spermatogonial cells. 双硫仑对小鼠精原细胞中乙醛基因毒性的影响。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/TCM.10003
E. Madrigal-Bujaidar, N. Velázquez-Guadarrama, P. Morales-Ramírez, M. Mendiola
{"title":"Effect of disulfiram on the genotoxic potential of acetaldehyde in mouse spermatogonial cells.","authors":"E. Madrigal-Bujaidar, N. Velázquez-Guadarrama, P. Morales-Ramírez, M. Mendiola","doi":"10.1002/TCM.10003","DOIUrl":"https://doi.org/10.1002/TCM.10003","url":null,"abstract":"The initial purpose of the study was to determine the potential of acetaldehyde (Ace) to increase the rate of sister-chromatid exchanges (SCEs) in mouse spermatogonia. We tested four doses of Ace (from 0.4 to 400.0 mg/kg), including a negative and a positive control group (distilled water and cyclophosphamide, respectively). The results showed that all tested doses were SCE inducers. The highest tested dose increased the control level more than three times. Also, the cumulative frequencies of SCEs per cell were higher in the Ace-treated animals than in the control cells. Ace is transformed into acetate through the enzyme aldehyde dehydrogenase, a process that may be blocked by disulfiram (Dis) generating the accumulation of Ace. The second purpose of the study was to determine if the administration of Dis (150 mg/kg) could increase the SCE rate produced by non-genotoxic doses of Ace. (0.004 and 0.04 mg/kg). The animals treated with the two doses of Ace alone showed no increase in the frequency of SCEs; also, Dis by itself was not an SCE inducer. However, the groups of animals previously treated with Dis showed an increase of 31 and 60% with respect to the values obtained with the two doses of Ace alone. Furthermore, the cumulative frequencies of SCEs per cell were higher in the animals administered with both compounds together than in those treated with them separately. These results suggest the need to extend this type of study to other models.","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"47 1","pages":"83-91"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87380942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Teratogenic effects of N-ethyl-N-nitrosourea (ENU) on larvae of the self-fertilizing fish Rivulus marmoratus (Cyprinodontiformes, Rivulidae). n -乙基-n -亚硝基脲(ENU)对自受精卵marmoratus鲤幼鱼的致畸作用。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/tcm.10031
Jae-Seong Lee, Sung Yeoul Chang, Il-Chan Kim, Myung-Soo Han, Young-Sik Lee, Yong-Sung Lee
{"title":"Teratogenic effects of N-ethyl-N-nitrosourea (ENU) on larvae of the self-fertilizing fish Rivulus marmoratus (Cyprinodontiformes, Rivulidae).","authors":"Jae-Seong Lee,&nbsp;Sung Yeoul Chang,&nbsp;Il-Chan Kim,&nbsp;Myung-Soo Han,&nbsp;Young-Sik Lee,&nbsp;Yong-Sung Lee","doi":"10.1002/tcm.10031","DOIUrl":"https://doi.org/10.1002/tcm.10031","url":null,"abstract":"<p><p>We showed that N-Ethyl-N-Nitrosourea (ENU) induces teratogenesis in larvae of the self-fertilizing fish Rivulus marmoratus. We discuss this and the issue of carcinogenesis caused by ENU.</p>","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"22 5","pages":"363-7"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/tcm.10031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21972532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
Fetotoxicity caused by the interaction between zinc and arsenic in mice. 小鼠锌和砷相互作用引起的胎儿毒性。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/tcm.10026
Maria Luiza Fascineli, E Sidney Hunter, Wilma De Grava Kempinas
{"title":"Fetotoxicity caused by the interaction between zinc and arsenic in mice.","authors":"Maria Luiza Fascineli,&nbsp;E Sidney Hunter,&nbsp;Wilma De Grava Kempinas","doi":"10.1002/tcm.10026","DOIUrl":"https://doi.org/10.1002/tcm.10026","url":null,"abstract":"<p><p>Arsenic is an environmental pollutant that induces congenital malformations in experimental models and can contribute to human birth defects. The environmental exposure to arsenic is relatively small when compared with the doses required to cause teratogenicity in mice and other laboratory animals. In order to study the action of zinc in the arsenic-induced teratogenicity, in the present work mice were either pretreated with zinc and later with arsenic or were treated simultaneously with zinc and arsenic in vivo and in vitro. Following administration of arsenate on gestation day 8, pregnant females were killed on the 17th day of gestation; maternal and fetal data were collected by laparotomy and used to calculate reproductive parameters. Fetuses were analyzed for the presence of external malformation and, after the appropriate processing, visceral and skeletal analyses were accomplished. Conceptuses were exposed in whole embryo culture to arsenicals on gestation day 8 (3-6 somite stage). After a 26 h culture period, morphological development was assessed. Neither pretreatment with zinc nor simultaneous administration of zinc prevented arsenic teratogenicity in these experimental models.</p>","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"22 5","pages":"315-27"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/tcm.10026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21972592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
Rat ventral prostate microsomal biotransformation of ethanol to acetaldehyde and 1-hydroxyethyl radicals: its potential contribution to prostate tumor promotion. 大鼠腹侧前列腺微粒体乙醇向乙醛和1-羟乙基自由基的生物转化:其促进前列腺肿瘤的潜在贡献。
Teratogenesis, carcinogenesis, and mutagenesis Pub Date : 2002-01-01 DOI: 10.1002/tcm.10028
G D Castro, A M A Delgado de Layño, M H Costantini, J A Castro
{"title":"Rat ventral prostate microsomal biotransformation of ethanol to acetaldehyde and 1-hydroxyethyl radicals: its potential contribution to prostate tumor promotion.","authors":"G D Castro,&nbsp;A M A Delgado de Layño,&nbsp;M H Costantini,&nbsp;J A Castro","doi":"10.1002/tcm.10028","DOIUrl":"https://doi.org/10.1002/tcm.10028","url":null,"abstract":"<p><p>Rat ventral prostate microsomal fraction was able to biotransform ethanol to acetaldehyde and 1-hydroxyethyl radicals (1HEt) in the presence of NADPH and oxygen. The enzymatic processes involved were not inhibited by desferrioxamine, CO, SKF 525A, 4-methylpyrazole, or polyclonal antibody against P450 reductase but they were significantly inhibited by diethyldithiocarbamate, 2-mercapto-1-methylimidazol, thiobenzamide, or diphenyleneiodonium chloride. Results would suggest the partial participation in these ethanol bioactivation processes of flavin containing monooxygenase (FMO) and/or other flavin dependent oxidases/peroxidases and of a non-iron metal-containing enzymes. Acetaldehyde and free radicals production by prostate microsomal fraction might potentially contribute to tumor promotion in heavy alcohol drinkers.</p>","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"22 5","pages":"335-41"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/tcm.10028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21972594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
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