Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention  Susan G. Komen for the Cure-AACR Outstanding Investigator Award for Breast Cancer Research
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Cell Growth & Differentiation

[Cancer Research 40, 2170-2173, July 1, 1980]
© 1980 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Banerjee, S.
Right arrow Articles by Oruambo, F. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Banerjee, S.
Right arrow Articles by Oruambo, F. I.

Microsome-mediated Covalent Binding of 1,2-Dichloroethane to Lung Microsomal Protein and Salmon Sperm DNA1

Sipra Banerjee, Benjamin L. Van Duuren and Felix Ibiba Oruambo

Laboratory of Organic Chemistry and Carcinogenesis, Institute of Environmental Medicine, New York University Medical Center, New York, New York 10016

In order to determine whether the covalent binding of the carcinogen 1,2-dichloroethane to macromolecules is dependent on microsomes or cytosol, microsomes and cytosol from lungs of C57BL/6 x C3H/He F1 (hereafter called B6C3F1) mice and Osborne-Mendel rats were incubated with [1,2-14C]dichloroethane and salmon sperm DNA. 1,2-Dichlorothane binds covalently to microsomal protein and DNA only in the presence of microsomes, whereas cytosol has insignificant metabolic activation. The binding to macromolecules was significantly higher in the presence of native microsomes than denatured microsomes. The interaction of 1,2-dichloroethane with DNA was enhanced following pretreatment of the animals with phenobarbital and 3-methylcholanthrene. On the other hand, glutathione reduced the binding. The binding of 1,2-dichloroethane to lung microsomal protein of B6C3F1 mice and to DNA was three and five times higher, respectively, than that of Osborne-Mendel rat lung microsomal proteins. 1,2-Dichloroethane interacts 85% and 100% more with protein and DNA, respectively, in the presence of microsomes obtained from lung than from liver of B6C3F1 mice. These results suggest a correlation between the microsomally mediated binding and species and organ susceptibility to 1,2-dichloroethane-induced tumorigenesis.

1 Supported by National Science Foundation Grant PFR76-10656 and by USPHS Grants ES-00260 and CA-13343.

Received 1/23/80. Accepted 3/27/80.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Cell Growth & Differentiation
Copyright © 1980 by the American Association for Cancer Research.