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Introduction: Methomyl (MET) is a carbamate insecticide, used in agriculture and public health to eliminate harmful insects. Besides its advantages in agriculture, it causes neurotoxic effects. The aim of this study was to evaluate the effect of MET on Spatial Working Memory (SWM), oxidative stress parameters, and histopathological changes in the hippocampus, as well as the possible protective role of Pelargonium graveolens Essential Oil (EO). Methods: Male Wistar rats were randomized into four groups of six animals: group I as the control that received the vehicle; group II received EO (75 mg/kg b.w), group III received MET (2 mg/kg b.w); and group IV received both MET and EO. The rats were administered the respective doses orally by gavage for 28 days. SWM was assessed using Y-maze on the day before the first treatment and day 28 after the last dose. They were sacrificed by decapitation and their brains were taken for assessing oxidative stress parameters and histopathological analysis. Results: MET treatment caused SWM deficits. Furthermore, drastic changes were observed in aspartate transaminase, alanine aminotransferase, and alkaline phosphatase activities. The level of malondialdehyde significantly increased, whereas antioxidant (glutathione-S-transferase and catalase) enzyme activities significantly decreased. The CA1 region of the hippocampus of rats exposed to MET revealed severe histological alterations. However, supplementation with EO improved SWM and partially restored the activities of antioxidant systems and prevented neuronal cell damage. Conclusion: P. graveolens EO has the potential in mitigating most of the adverse effects in the hippocampus and prevents SWM impairment induced by MET toxicity.

Mannoproteins, as the main constituents of the outer layer of yeast cell walls, are able to interact with phagocytic cells in an opsonin-independent manner through the mannose receptor (MR) and to induce yeast ingestion by the professional phagocytes. Moreover, the MR also mediates endocytosis of soluble ligands through clathrin-coated pits. Here, we studied some aspects of the interaction between the MR and Candida albicans using murine E-clone macrophages and the consequences on MR trafficking. Using a pull-down assay involving mixture E-clone macrophage detergent lysate with mannosylated Sepharose beads and glutaraldehyde-fixed, heat-killed (HK) C. albicans, we found that binding of solubilized MR to mannosylated particles occurred with characteristics similar to the receptor's cell-surface mannose-binding activity. We then demonstrated that MR expressed on E-clone macrophages contributed to phagocytosis of unopsonized, HK C. albicans and that yeast phagocytosis induced a decrease in MR endocytic activity without concomitant degradation of the receptor in the time lapse studied.

We studied the involvement of lectin-like receptors in phagocytosis of unopsonized heat-killed yeast (Saccharomyces cerevisiae) by murine macrophage-like cell lines and murine peritoneal resident macrophages. For this purpose we used a technique that allowed us to discriminate ingested and adsorbed heat-killed yeast. The internalization can be partly inhibited by soluble polyosides such as laminarin (beta-glucan) or alpha-mannan. However, when they were used together (0.4 mg/ml alpha-mannan and 0.4 mg/ml laminarin), almost complete inhibition of phagocytosis was obtained. These observations suggest that phagocytosis of unopsonized heat-killed yeast by murine macrophage-like cell lines as well as murine peritoneal resident macrophages is mediated by both mannose and beta-glucan receptors. The respective activity of these two types of receptors is a function of in vitro cell differentiation. To achieve maximal phagocytosis of unopsonized heat-killed yeast, coexpression of both mannose and beta-glucan receptors is required.