In addition, the limited absorption of fenbendazole from the intestine results in low levels of the drug and its active metabolites in tissue relative to the levels within the gut, to which the targeted parasites are exposed ( 1, 14, 15). As we researched this proposed prophylactic treatment, we became concerned that the fenbendazole-containing chow might compromise our experiments, but also became intrigued by the possibility that this drug might have antineoplastic effects, by disrupting the tubulin microtubule equilibrium, or by altering the viability or radiosensitivity of cells in the hypoxic environments found in solid tumors.įenbendazole acts on helminthes primarily by binding to tubulin and disrupting the tubulin microtubule equilibrium its utility as an antiparasitic drug results from differences in the structures of tubulin in mammalian cells and in lower organisms, which lead to its greater binding to tubulin, and therefore greater inhibition of polymerization, in the parasites ( 11– 13). Our research uses tumors in rats and mice to evaluate the effects of new regimens for treating solid tumors with radiation and/or anticancer drugs ( 4– 10). We became interested in fenbendazole when our university veterinarians recommended that all experimental rodents, including uninfected colonies such as ours, be treated with a fenbendazole-containing diet because of pinworm infections in some colonies. Fenbendazole, carbamic acid methyl ester, is widely used to treat pinworms, other helminthes, and a variety of parasitic infections in laboratory animals, livestock, companion animals, and people ( 1– 3).
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