Literature DB >> 884659

Induction of aryl hydrocarbon hydroxylase and forestomach tumors ben benzo(a)pyrene.

A J Triolo, G E Aponte, D L Herr.   

Abstract

While papillomatous tumors developed in the forestomach of female Ha/ICR mice after a 12-week chronic feeding period of benzo(a)pyrene (BP), no tumors developed in the glandular portion of stomach or in the lung or liver. Among all tissues examined, the forestomach showed the greatest increase of aryl hydrocarbon hydroxylase (AHH) activity following acute or chronic administration of BP. Single acute doses of BP induced AHH activity in forestomach, glandular stomach, lung, and small intestine, but not in the kidney and liver of these animals. Similarly, after chronic administration of BP, AHH activity was inducible in the forestomach, glandular stomach, and lung, but again not in the liver. Although the formation of tumors is associated with greater inducibility of AHH activity in the forestomach after BP administration, the relationship between tissue inducibility of AHH activity and susceptibility to BP carcinogenesis is still not clear. Further studies regarding the formation of specific carcinogenic epoxides of BP in itssues both susceptible (e.g., forestomach) and resistant to BP carcinogenesis would more clearly define the relationship between AHH inducibility and BP carcinogenesis.

Entities:  

Mesh:

Substances:

Year:  1977        PMID: 884659

Source DB:  PubMed          Journal:  Cancer Res        ISSN: 0008-5472            Impact factor:   12.701


  3 in total

1.  Conjugation of 1-naphthol in human gastric epithelial cells.

Authors:  P Déchelotte; M Varrentrapp; H J Meyer; M Schwenk
Journal:  Gut       Date:  1993-02       Impact factor: 23.059

2.  Dietary mutagen exposure and risk of pancreatic cancer.

Authors:  Donghui Li; Rena Sue Day; Melissa L Bondy; Rashmi Sinha; Nga T Nguyen; Douglas B Evans; James L Abbruzzese; Manal M Hassan
Journal:  Cancer Epidemiol Biomarkers Prev       Date:  2007-04       Impact factor: 4.254

3.  Interaction of the cytochrome P4501A2, SULT1A1 and NAT gene polymorphisms with smoking and dietary mutagen intake in modification of the risk of pancreatic cancer.

Authors:  Hideo Suzuki; Jeffrey S Morris; Yanan Li; Mark A Doll; David W Hein; Jun Liu; Li Jiao; Manal M Hassan; Rena S Day; Melissa L Bondy; James L Abbruzzese; Donghui Li
Journal:  Carcinogenesis       Date:  2008-05-21       Impact factor: 4.944

  3 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.