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Concanavalin A (Con A) immobilized monosize and magnetic poly(glycidyl methacrylate)[m-poly(GMA)] beads were investigated for specific adsorption of yeast invertase from aqueous solutions. m-Poly(GMA) beads (1.6 µm in diameter) were prepared by dispersion polymerization in the presence of Fe 3 O 4 nanopowder. The epoxy groups of m-poly(GMA) beads were opened by base catalyses. Then, Con A was immobilized by covalent binding onto the beads. Con A immobilization amount was 12.5 mg/g. The invertase adsorption capacity of the m-poly(GMA)/Con A beads was 111 mg/g. The maximum invertase adsorption on the m-poly(GMA)/Con A beads was observed at pH 5.5. The optimum activity for both free and adsorbed invertase was observed at 50 • C. V max values were determined as 330 U/mg and 292 U/mg enzyme, for free and adsorbed invertase, respectively. K M values were found to be the same for free and adsorbed invertase (20 mM). Adsorption of invertase via Con A improved the pH stability of invertase. Thermal stability also increased with adsorption. The adsorbed enzyme activity was found to be quite stable in repeated experiments.

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Epilepsy is a common brain disorder that seizures could cause neuronal loss in the hippocampus. Oxidative stress has an important role in the pathology of this way. The aim of this study was to investigate the neuroprotective effect of astaxanthin (ATX), on pentylenetetrazole (PTZ) induced epileptic seizures in rats and in SH-SY5Y human neuroblastoma cell culture. Method: In our study, we used 42 male 230-250 g Wistar Albino rats. Animals were divided into seven groups as control, saline (PTZ; 1 ml/kg serum physiologic), positive control (2,5 mg/kg diazepam), 10 mg/kg, 20 mg/kg, 40 mg/kg and 80 mg/kg ATX for seven days. Thirty min after the administration of the last drug at the indicated doses, PTZ was administered 45 mg/kg to induce an epileptic seizure. The animals were observed for 30 min. Seizure stages according to the Racine Scale (RC) and first myoclonic jerk times (FMJ). Twenty four hours after PTZ injection, passive avoidance test was performed, and then brain tissues were removed for biochemical and histopathological evaluation. The hippocampal Cornu Ammonis 1 (CA1), CA3 and dentate gyrus (DG) regions were evaluated histopathologically regarding neuronal damage. Besides, oxidative stress markers total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI)) were measured in brain tissues. Furthermore, ATX was performed in vitro SH-SY5Y human neuroblastoma cell culture to evaluate PTZ-induced neurotoxicity. Results: When epileptic behaviors were evaluated, ATX did not affect RC and FMJ (p>0, 05). However, ATX reduced both cognitive impairment in passive avoidance test and neuronal damage in the hippocampus (p<0, 05). Moreover, ATX reduced both TOS levels and OSI in the brain (p<0, 05). Besides of these in vitro studies, ATX increased neuronal viability in vitro. Conclusions: Although ATX does not have antiepileptic properties directly, it has a protective effect on not only in vivo but also in vitro. These effects may occur by possible oxidative pathways.

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