Resumen:
osinophils (Eo) are typically associated with immune response to helminth. Previously, we demon-strated 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 signif-icant 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 hydrogen peroxide, which precedes mitochondrial
injury and leads again to apoptosis. Finally, we demonstrated the participation of hydrogen peroxide in
the peritoneal Eo apoptosis in vivo, both during the early stages of experime