Oxfendazole induces protein catabolism and gluconeogenesis in experimental neurocysticercosis.

Neurocysticercosis (NCC) is an endemic public health disease of the central nervous system highly related to epilepsy and seizures. Taenia crassiceps is an experimental model used for NCC and biochemical studies of the host-parasite relationship. For the past 50 years the NCC therapeutic treatment is performed with albendazole (ABZ) and praziquantel which opens a gap for new therapies due to parasitic resistance and other adverse effects of the drugs. Oxfendazole (OXF) is an albendazole derivative with efficacy against tissue cestodes of veterinary importance. The aim of this study was to determine the metabolic impact of OXF on T. crassiceps cysticerci intracranially inoculated in Balb/C mice. The animals were intracranially inoculated with T. crassiceps cysticerci and 30 days later received single dose oral treatment of OXF, ABZ and NaCl 0.9% (control group). The metabolic impact was quantified through the detection of metabolites from glycolysis, anaerobic fermentation of lactate and propionate, tricarboxylic acid cycle, protein catabolism, fatty acids oxidation. The differences observed in the concentrations of metabolites from the OXF treated group showed that the drug induced gluconeogenesis, increase in protein catabolism, fatty acids oxidation and propionate fermentation in comparison to the ABZ and control treated groups. In conclusion, OXF induced greater metabolic impact in T. crassiceps cysticerci than the standard NCC treatment, ABZ, showing that it may represent an alternative drug for its treatment.