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Oltipraz, an Inhibitor of Human Immunodeficiency Virus Type 1 Replication
Hans J. Prochaska, Yong Yeh, Penny Baron and Bruce Polsky
Proceedings of the National Academy of Sciences of the United States of America
Vol. 90, No. 9 (May 1, 1993), pp. 3953-3957
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/2361870
Page Count: 5
You can always find the topics here!Topics: HIV 1, Enzymes, Cell lines, Carcinogenesis, Thiols, Viruses, Infections, Cancer, Isothiocyanates, Cultured cells
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Glutathione depletion may play a pivotal role in the pathogenesis of human immunodeficiency virus type-1 (HIV-1) infection. Since certain compounds prevent experimental carcinogenesis by elevating the levels of glutathione and phase II detoxication enzymes, we compared the potencies of several inducers with their ability to inhibit basal levels of HIV-1 replication in H9 cutaneous T-cell lymphoma cells. All monofunctional inducers tested elevated the levels of glutathione and quinone reductase, a marker for phase II enzyme induction. However, only oltipraz [4-methyl-5-(2-pyrazinyl)-1,2-dithiole-3-thione] was effective at inhibiting HIV-1 replication (IC50 = 14.8 ± 3.1 μ M). The antiviral effect of oltipraz was potentiated by 3'-azido-3'-deoxythymidine. Thus, 1,2-dithiole-3-thiones represent a hitherto unrecognized class of anti-HIV-1 agents. Oltipraz behaves kinetically as an irreversible inhibitor of HIV-1 reverse transcriptase in the template-primer binding domain. Oltipraz has been used to treat schistosomiasis in humans and is undergoing clinical evaluation as an anticarcinogen. Thus, oltipraz (and other 1,2-dithiole-3-thiones) may have therapeutic utility in HIV-1-infected individuals, not only because of their antiretroviral activity, but also by preventing the development of HIV-1-associated neoplasms.
Proceedings of the National Academy of Sciences of the United States of America © 1993 National Academy of Sciences