Recently, we introduced an epoxy group to mebendazole by a reaction with epichlorohydrin and obtained two isoforms, mebendazole C1 (M-C1) and mebendazole C2 (M-C2). The in vitro effects of mebendazole derivatives at different concentrations on Echinococcus multilocularis protoscoleces and metacestodes as well as cytotoxicity in rat hepatoma (RH) cells were examined. The results demonstrated that the solubility of the two derivatives was greatly improved compared to mebendazole. The mortality of protoscoleces in vitro reached to 70–80% after 7 days of exposure to mebendazole or M-C2, and M-C2 showed higher parasiticidal effects than mebendazole (P > 0.05). The parasiticidal effect of M-C1 was low, even at a concentration of 30 µm. The percentage of damaged metacestodes that were treated with mebendazole and M-C2 in vitro at different concentrations were similar, and M-C1 exhibited insignificant effects on metacestodes. Significant morphological changes on protoscoleces and metacestodes were observed after treatment with mebendazole and M-C2. In addition, the introduction of an epoxy group to mebendazole also reduced its cytotoxicity in RH cells. Our results demonstrate that the introduction of an epoxy group not only improved the solubility of mebendazole, but also increased its parasiticidal effects on E. multilocularis and reduced its cytotoxicity in RH cells.

Background: Heavy ion radiation has more advantages than traditional radiation therapy in the treatment of cancer, mainly because of its superior biological effects. However, there is currently no reliable evidence that heavy ion radiation can induce cell death in hydatid cysts at the cellular and molecular level. In addition, we believe heavy ion therapy could be a potential alternative approach for the treatment of hydatid cysts. Methodology/Principal Finding: The hydatid cysts and protoscolices were obtained from an experimentally infected KunMing mice. LD50 was used to evaluate the death of the protoscolex. The cellular and ultrastructure of the parasites were observed under light and electron microscopes, the damage and copy numbers of mitochondrial DNA (mtDNA) were decided by QPCR. The apoptosis was evaluated by the expression and activity of caspase3. Dose-dependent ionizing radiation induced damage to the initial mtDNA. Echinococcosis cyst after ionizing radiation showed sparse cytoplasm, disorganized and clumped organelles, huge vacuoles, and villus deletions. The kinetic of DNA repair activity after X-ray irradiation was faster than those after carbon-ion irradiation. High doses of carbon ion radiation caused irreversible attenuation of mitochondrial DNA. Cysts showed obvious reduction in size after radiation. Carbon ion radiation was more effective than X-ray radiation in inhibiting hydatid cysts. Conclusions: These studies provide evidence that heavy-ion radiation can cause the extinction of hydatid cysts in vitro. The carbon-ion radiation is more advantageous than X-ray radiation in suppress hydatid cyst.