Resumen:
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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 E