Relationship between antioxidant defense in Acanthamoeba spp. infected lungs and host immunological status.

The role of oxidative stress in the pathogenicity of acanthamoebiasis is an important aspect of the intricate and complex host-parasite relationship. The aim of this experimental study was to determine oxidative stress through the assessment of lipid peroxidation product (LPO) levels and antioxidant defense mechanism in Acanthamoeba spp. lung infections in immunocompetent and immunosuppressed hosts. In Acanthamoeba spp. infected immunocompetent mice we noted a significant increase in lung lipid peroxidation products (LPO) at 8 days and 16 days post infection (dpi). There was a significant upregulation in lung LPO in immunocompetent and immunosuppressed mice infected by Acanthamoeba spp. at 16 dpi. The superoxide dismutase activity decreased significantly in lungs in immunosuppressed mice at 8 dpi. The catalase activity was significantly upregulated in lungs in immunocompetent vs. immunosuppressed group and in immunocompetent vs. control mice at 16 dpi. The glutathione reductase activity was significantly lower in immunosuppressed group vs. immunosuppressed control at 24 dpi. We found significant glutathione peroxidase downregulation in immunocompetent and immunosuppressed groups vs. controls at 8 dpi, and in immunosuppressed vs. immunosuppressed control at 16 dpi. The consequence of the inflammatory response in immunocompetent and immunosuppressed hosts in the course of experimental Acanthamoeba spp. infection was the reduction of the antioxidant capacity of the lungs resulting from changes in the activity of antioxidant enzymes. Therefore, the imbalance between oxidant and antioxidant processes may play a major role in pathology associated with Acanthamoeba pneumonia.

The effect of low levels of lead (Pb) in the blood on levels of sphingosine-1-phosphate (S1P) and expression of S1P receptor 1 in the brain of the rat in the perinatal period.

Sphingolipids are the main components of the lipid membrane. They also perform structural functions and participate in many signal transmission processes. One of the bioactive sphingolipids is sphingosine-1-phosphate (S1P), a ligand for five G protein-coupled receptors (S1PRs1-5), which can also act as an intracellular second messenger. S1P is responsible for the stimulation of progenitor cells in the brain, but it can also induce apoptosis of mature neurons. This study is aimed at assessing the effect of pre- and neonatal exposure to permissible Pb concentrations on S1P levels and S1PR1 (EDG1) expression in the prefrontal cortex, cerebellum, and hippocampus of rats. The concentrations of S1P were determined by RP-HPLC, S1PR1 expression was determined by RT PCR and Western Blot, and receptor immunolocalization was determined by immunohistochemistry method. Our results showed that even low blood Pb concentrations, i.e. within the acceptable limit of 10 µg/dL caused changes in the concentration of S1P in the cerebellum, prefrontal cortex, and hippocampus. Our data also showed a significant decrease in the level of S1PR1 in all studied part of brain, without significant changes in S1PR1 gene expression. Pre- and neonatal exposure to Pb also resulted in a decrease in the expression of S1PR1 in glial cells in all regions of the Cornu Ammonis (CA1-CA4) and Dentate Gyrus in the hippocampus, as well as in all layers of the cerebellum and prefrontal cortex, compared to the unexposed control group.