Context: Praziquantel (PZQ) is a highly efficacious anthelmintic against many flatworms including schistosomes. PZQ has been in use for more than 25 years, and concern is increasing that resistance has emerged in human schistosomes in Egypt and other endemic countries. Objective: The current study was designed to evaluate a recently described method for induction of PZQ resistance in Schistosoma mansoni. Materials and methods: Successive subcurative drug treatments of Biomphalaria alexandrina snails infected with an Egyptian strain of S. mansoni were undertaken. Cercariae shed from snails exposed and unexposed to PZQ were used to infect mice. Forty-five days after infection, mice were treated with a single oral dose of PZQ in 2% aqueous solution of Cremophor-EL Õ . The concentration of PZQ was 0, 200, 400, or 800 mg/kg. Thirty-three days after treatment, all groups of mice were dissected to collect the S. mansoni worms by the perfusion technique. In addition, the oogram pattern was examined to study the production, maturity, and death of S. mansoni eggs in the different groups of mice. Results: The present study has shown that the sublethal dose for induction of PZQ resistance in the intra-molluscan S. mansoni stages was 500 mg/kg. The worm count and the percentage of immature eggs in different groups of mice were significantly affected by the intra-molluscan exposure to PZQ and the drug concentration used to treat infected mice. Discussion and conclusion: The results obtained herein confirm the possibility of using successive drug treatments of infected B. alexandrina to induce PZO resistance in S. mansoni.

The aim of the present study was to investigate the effect of triclabendazole (CAS 68786-66-3) therapy alone or in combination with ascorbic acid (vitamin C, CAS 50-81-7) and tocofersolan (vitamin E, CAS 30999-06-5), in Fasciola hepatica patients, on Lipo-peroxidation (LPO) and blood antioxidant capacity. 32 Fasciola hepatica patients were divided into two groups (16 acute and 16 chronic). Each group was divided into two subgroups of 8 patients each. One subgroup was given two consecutive oral doses each of 10 mg/kg body weight of triclabendazole suspension and the other received vitamin C (1000 mg/day) and vitamin E (600 mg/day) for two months, together with the same dose of triclabendazole given to the first subgroup. Ten healthy subjects served as controls. The results revealed a significant increase in serum and erythrocyte lipid peroxide levels and a significant decrease in glutathione levels as well as in glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in all study groups compared to their corresponding control values. After triclabendazole treatment, pronounced improvements in all studied parameters were observed which could be attributed to the fasciolicidal effect of the drug. The significant improvement of SOD and GPX activities and in lipid peroxide levels after vitamins supplementation as compared to their corresponding values after treatment with triclabendazole alone could be explained on the basis of the potent action of these vitamins in protection against oxidative damage.

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