ArticleParasitology research2017
In vivo treatment with nitazoxanide induces anaerobic metabolism in experimental intraperitoneal cysticercosis.
Article in Parasitology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 8 citations in OpenAlex.
- Nitazoxanide Exhibits Schistosomicidal Activity Against Schistosomula and Adult Schistosoma mansoni and Influences Praziquantel-Associated Outcomes.Acta parasitologica · 2026Article
- In Vivo Treatment with the Combination of Nitazoxanide and Flubendazole Induces Gluconeogenesis and Protein Catabolism in Taenia crassiceps cysticerci.Acta parasitologica · 2021Article
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7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Taenia crassiceps cysticerci are used as experimental model to study the host-parasite relationship and treatment of cysticercosis. One of the described mode of actions of nitazoxanide (NTZ) is to block the pyruvate ferredoxine oxidoreductase (PFOR) enzyme which is an essential enzyme to the parasite metabolism. The aim of this study was to determine the in vivo influence of one dosage of NTZ on the energetic metabolism of T. crassiceps cysticerci. Thirty days after the intraperitoneal inoculation of T. crassiceps cysticerci, BALB/c mice were orally treated with 7.5 mg/kg of NTZ. The control group was treated with physiologic solution (NaCl 0.9%). After 24 h, the animals were euthanized and the cysticerci were removed, washed, and processed for biochemical analysis. The organic acids detection occurred through high-performance liquid chromatographic and spectrophotometric analysis. While there was no difference in the glucose dosages, it was possible to observe a significant increase in the lactate concentrations and a decrease in the pyruvate concentrations of the NTZ-treated groups when compared to the control group. Also, there was a decrease in the urea and alpha-ketoglutarate concentrations. This probably occurred due to the impairment of the parasite's PFOR and nitroreductases leading an impairment of the mitochondrial aerobic pathways. In conclusion, the in vivo NTZ treatment leads to an increase in the lactic fermentation and to a decrease in the protein catabolism in T. crassiceps cysticerci.
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