Journal Article

Acrylonitrile-induced morphological transformation in Syrian hamster embryo cells

Haizhou Zhang, Lisa M. Kamendulis, Jiazhong Jiang, Yong Xu and James E. Klaunig

in Carcinogenesis

Volume 21, issue 4, pages 727-733
Published in print April 2000 | ISSN: 0143-3334
Published online April 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.4.727
Acrylonitrile-induced morphological transformation in Syrian hamster embryo cells

More Like This

Show all results sharing this subject:

  • Clinical Cytogenetics and Molecular Genetics

GO

Show Summary Details

Preview

Acrylonitrile (ACN) is a monomer used in the synthesis of rubber, fibers and plastics. Previous studies demonstrated that ACN induces brain neoplasms (predominately astrocytomas) in rats following chronic treatment. While the mechanisms of ACN-induced glial cell carcinogenicity have not been completely elucidated, investigations by our group and others have suggested a role for the induction of oxidative stress and the resultant oxidative damage in this process. In vitro cell transformation models are useful for detecting and studying the mechanisms of chemical carcinogenesis. Cell transformation by chemical carcinogens in Syrian hamster embryo (SHE) cells exhibits a multistage process similar to that observed in vivo, for both non-genotoxic and genotoxic carcinogens. In the present study, the ability of ACN to induce morphological transformation and oxidative damage was examined in SHE cells. ACN induced an increase in morphological transformation at doses of 50, 62.5 and 75 μg/ml (maximum sub-toxic dose tested) following 7 days of continuous treatment. SHE cells exposed to ACN for 24 h failed to increase morphological transformation. Morphological transformation by ACN was inhibited by co-treatment with the antioxidants α-tocopherol and (–)-epigallocathechin-3 gallate (EGCG) for 7 days. Treatment of SHE cells with 75 μg/ml ACN produced a significant increase in 8-hydroxy-2′-deoxyguanosine that was also inhibited by co-treatment with α-tocopherol or EGCG. These results support the proposal that oxidative stress and the resulting oxidative damage is involved in ACN-induced carcinogenicity.

Keywords: ACN, acrylonitrile; B[a]P, benzo[a]pyrene; CEO, 2-cyanoethylene oxide; 2′-dG, 2′-deoxyguanosine; DMEM-L, DMEM LeBoeuf's modification; DMSO, dimethylsulfoxide; EGCG, (–)-epigallocathechin-3 gallate; GSH, reduced glutathione; OH8dG, 8-hydroxy-2′-deoxyguanosine; ROS, reactive oxygen species; SHE, Syrian hamster embryo.

Journal Article.  5610 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.