Abstract

POLYRIBOINOSINIE-POLYRIBOCYTIDYLIC acid, poly(rI).poly(rC), inhibits the multiplication of oncogenic viruses, the cellular transformation induced by these viruses and the development of virus-induced tumours in animals1, 2. The effect of the synthetic double-stranded RNA against viruses is possibly mediated by the induction of interferon3. Poly(rI).poly(rC)4, 5 and interferon6 have also been shown to inhibit chemically induced tumorigenesis in mice. This effect, however, is difficult to interpret because of other known actions of the synthetic polynucleotide. Thus, it is known that poly(rI).poly(rC) non-specifically enhances macrophage activity and lymphocyte cytotoxicity1, 7, 8 and influences the activity of microsomal drug-metabolising enzymes9, 10 which convert most chemical carcinogens into the reactive metabolites, the ultimate carcinogens11. Moreover, the high toxicity of poly(rI).poly(rC) in mice could conceivably contribute to its capacity to inhibit the growth of chemically induced tumours.

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