P-GLYCOPROTEIN IMMUNOLOCALIZATION AND GLUTATHION-S-TRANSFERASE ACTIVITY IN Fasciola hepatica RECOVERED FROM TRICLABENDAZOLE TREATED SHEEP

SOLANA H., SCARCELLA S.; ALZOLA R. & LANUSSE C

Leipzig, germany

Congreso; 11Th International Congress of the European Association for Veterinary pharmacology and Toxicology (EAVPT); 2009

EAVPT

Fasciolasis is a zoonotic parasitic disease caused by Fasciola hepatica. Its control is based on the use of triclabendazole (TCBZ), an halogenated benzimidazole thiol derivative which shows excellent efficacy against both juvenile (immature) and adult stages. TCBZ is metabolised into its anthelmintically active sulphoxide metabolite (TCBZSO) by the host liver [1] but also by the parasite’s subcellular fractions [2]. It has been reported that F. hepatica had significantly higher sulphoxidative activity compared to nematode and cestode parasites [3] Parasite resistance to different anthelmintics is growing worldwide, including the resistance of F. hepatica to TCBZ. The helminth parasites possess different biochemical mechanisms for detoxification. Overall, helminth parasites may evade drug antiparasitic effects by: i) mutation of target molecules, ii) overexpression of efflux pumps, i.e. P glycoprotein  (P-gp), and/or iii) overexpression of metabolic enzymatic systems, i.e Glutathion-S-transferase (GST). Hence, the knowledge of detoxification and resistance mechanisms in F. hepatica is needed. This work was aimed to assess the expression and tissue distribution of P-gp and the enzymatic activity of GST in adult F. hepatica specimens recovered from TCBZ treated sheep.