Antioxidant capacity in rat brain after ICV treatment with streptozotocin and alloxan — a preliminary study
Aida Šapčanina, Emin Sofica✉, I Tahirovića, M. Salkovic-Petrisicb, Siegfried Hoyerc, Peter Franz Riedererd
- aDepartment of Chemistry, Faculty of Science, University of Sarajevo, Sarajevo, Bosnia and Herzegovina
- bDepartment of Pharmacology and Croatian Institute for Brain Research, School of Medicine, University of Zagreb, Zagreb, Croatia
- cDepartment of Pathology, University Clinic, University of Heidelberg, Heidelberg, Germany
- dDepartment of Clinical Neurochemistry, Clinic and Policlinic for Psychiatry, University of Wuerzburg, Wuerzburg, Germany
- ✉Corresponding author
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Abstract
Intracerebroventricular (icv) administration of betacytotoxic drug streptozotocin (STZ) produces long-term and progressive cognitive deficits in rats, as well as deficits in cerebral glucose and energy metabolism. These changes resemble those found in the brain of patients with sporadic Alzheimer's disease (sAD), and therefore, STZ-icv treated rats have been proposed as an experimental model of sAD. In this study the antioxidant capacity (AC), using manual oxygen radical absorbance capacity (ORAC) assay, was measured in the rat brain frontoparietal cortex (FC) and brainstem-cerebellum region (BS-CB) after administration of STZ and another betacytotoxic drug alloxan (AL). Region-specific differences of AC were found, which were more expressed when hydroxyl radical (ORAC(-OHo)) generator was used in the assay. AC against ORAC(-OHo) was significantly lower in BS-CB than in FC of the control rats. Furthermore, ORAC(-OHo) significantly decreased in BS-CB 3-months following the icv administration of AL, but significantly increased following the TG+AL combined treatment in comparison with the controls. However, 3-months following the icv treatment of AL combination with a different glucose transport inhbitor, 3-O-methyl-D-glucose, ORAC(-OHo) values in BS-CB and ORAC(-ROOo) values in FC were significantly decreased in comparison to the controls. Our results suggest that betacytotoxic-icv treatment alters antioxidant defense systems in the brain, which particularly regarding the STZ-icv treatment, could be a useful tool in search for possible new antioxidant treatments of the neurodegenerative disorders such as sAD.