INVOLVEMENT OF A MITOCHONDRIAL PATHWAY AND KEY ROLE OF HYDROGEN PEROXIDE DURING EOSINOPHIL APOPTOSIS INDUCED BY EXCRETORY-SECRETORY PRODUCTS FROM FASCIOLA HEPATICA.

SERRADELL MC; GUASCONI L; MASIH DT

Elsevier

Lugar: Amsterdam; Año: 2009 vol. 163 p. 95 - 95

font lang="en" face="ArialUnicodeMS" size="3"> Eosinophils (Eo) are typically associated with immune response to helminth. Previously, we demonstrated that excretory-secretory products (ESP) from Fasciola hepatica induce eosinophil apoptosis by a caspase-dependent mechanism. In this study, we observed that ESP caused mitochondrial-membrane depolarization of eosinophils leading to the release of cytochrome c. Also, ESP induced an increase in the reactive oxygen species (ROS) production, which preceded the mitochondrial injury. We found a significant rise in hydrogen peroxide, but not in the anion superoxide levels. Furthermore, catalase, but not superoxide dismutase, inhibited the mitochondrial depolarization as well as apoptosis. So, ESP induce in Eo an early increase in the ROS production, mainly hydro