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[Cancer Research 15, 249-255, May 1, 1955]
© 1955 American Association for Cancer Research

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Tissue Autoxidation Inhibitors

I. The Inhibition of DOPA Autoxidation by Extracts from Normal and Neoplastic Tissues*

Herbert M. Hirsch

( Division of Cancer Biology, Department of Physiology, University of Minnesota Medical School, Minneapolis, Minn.)

An inhibitor of autoxidation in normal and neoplastic mouse tissues has been investigated, using the DOPA autoxidation system as an assay. Some properties of the assay system itself were studied. Addition of a commercial detergent speeded up the reaction rate and resulted in solubilization of melanin as it was formed from DOPA. The effect of a number of reducing, chelating, and complexing substances as well as of metal ions was tested, and the conclusion was reached that autoxidation of DOPA is probably due to traces of metals present. Both normal and neoplastic tissues contained a powerful inhibitor of DOPA autoxidation. Inhibition was greatest in concentrated extracts and was diminished on dilution. Inhibition appeared to be due to compounds tightly binding copper or other metal ions needed for the autoxidation of DOPA. The inhibitor in normal liver consisted mainly of a heat-labile, nondialyzable fraction, and a similar component was found in normal mammary tissue. The inhibitory action appeared due to specific compounds and not to the presence of protein in general, since several pure proteins tested did not give the effect. Protein-linked SH groups were not involved. The inhibitor in tumor tissue, on the other hand, consisted of a heat-labile, dialyzable and of a heat-stable, nondialyzable fraction. The possible importance and implications of such inhibitors in tissues are discussed.

* Assisted by a grant (C-2469) from the National Cancer Institute of the National Institutes of Health, Public Health Service, by a grant from the Minnesota Division of the American Cancer Society, and by a grant to Dr. J. J. Bittner from the National Cancer Institute, National Institutes of Health, U.S. Public Health Service.

Received 9/20/54.





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 Meeting Abstracts Online
Copyright © 1955 by the American Association for Cancer Research.