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Background: Neurological disorders suggest that the excitotoxicity involves a drastic increase in intracellular Ca 2+ concentrations and the formation of reactive oxygen species. The presence of these free radicals may also affect the dopaminergic system. The aim of this work was to determine if riboflavin (B 2 ) and pyridoxine (B 6 ) provide protection to the brain against free radicals generated by 3-nitropropionic acid (3-NPA) by measuring the levels of dopamine (DA) and selected oxidative stress markers., Methods: Male Fisher rats were grouped (n = 6) and treated as follows: group 1, control (NaCl 0.9%); group 2, 3-NPA (20 mg/kg); group 3, B 2 (10 mg/kg); group 4, B 2 (10 mg/kg) + 3-NPA (20 mg/kg); group 5, B 6 (10 mg/kg) and group 6, B 6  + 3-NPA. All treatments were administered every 24 h for 5 days by intraperitoneal route. After sacrifice, the brain was obtained to measure DA, GSH, and lipid peroxidation, Ca 2+ , Mg 2+ , ATPase and H 2 O 2 ., Main Findings: Levels of dopamine increased in cortex, striatum and cerebellum/medulla oblongata of animals that received 3-NPA alone. The lipid peroxidation increased in cortex, striatum, and cerebellum/medulla oblongata, of animals treated with B 2 vitamin alone. ATPase dependent on Ca +2 , Mg +2 and H 2 O 2 increased in all regions of animals that received 3-NPA alone., Conclusion: The results confirm the capacity of 3-NPA to generate oxidative stress. Besides, the study suggests that B 2 or B 6 vitamins restored the levels of DA and reduced oxidative stress in brain of rats. We believe that these results would help in the study of neurodegenerative diseases.

Purpose: The aim was to evaluate if morphine sulphate combined with cerebrolysin enhances the risk of oxidative damage in the presence of moderate hypoglycaemia., Methods: Wistar rats under starvation for 48h received a single dose of 215 mg/kg cerebrolysin or 4 mg/kg morphine sulphate. Glutathione (GSH) and 5-hydroxyindoleacetic acid (5-HIAA) levels were measured in brain tissue, as well as lipid peroxidation, Na(+)-K(+) ATPase and total ATPase enzymatic activities, by fluorescence and spectrophotometric methods., Results: GSH and 5-HIAA levels decreased significantly (p<0.05) in animals which received cerebrolysin and morphine alone or combined. TBARS levels increased in all groups, but the values were statistically significant only in those animals that received cerebrolysin combined with morphine (p<0.05). Na(+)-K(+) ATPase and total ATPase activities decreased significantly in rats treated only with morphine, but the cerebrolysin and morphine groups showed a significant increase in these enzymatic activities., Conclusions: Results suggest that cerebrolysin as well as morphine induced changes in cellular regulation and biochemical responses to oxidative stress induced by moderate hypoglycaemia in brain.

Objective: To evaluate the antioxidant effect of selenium on Na+, K(+)-ATPase in rat brain in the presence of nitric oxide., Methods: Male Wistar rats (70 g) were treated as follows: group 1 received 1 microg of i.p. sodium nitroprus-side per kg (SNP), group 2 received 5 microg sodium selenite during 20 days, group 3 received sodium selenite 5 microg + SNP 1 microg and the control group received vehicle 50 microl (0.9% NaCl), same period and route. At the end of treatment, animals were sacrificed and their brain dissected into cortex, hemispheres, cerebellum and brain stem in order to determine lipid peroxidation (TBARS), Na+, K+ ATPase and total ATPase in each section. Blood hemoglobin concentration (Hb) and prostate weight were also assessed., Results: A significant increase of Hb in blood and of proteins in cortex and hemisphere was detected, but TBARS values fell due to the effect of sodium selenite in all examined regions, except for cerebellum. ATPase activity declined in all groups and regions with and without NTP. We conclude that diet supplementary selenium to inhibit NO generation can be a useful treatment in chronic inflammatory diseases.

Background: Diabetic retinopathy (DR) is one of the main complications in patients with diabetes and has been the leading cause of visual loss since 1990. Oxidative stress is a biological process resulting from excessive production of reactive oxygen species (ROS). This process contributes to the development of many diseases and disease complications. ROS interact with various cellular components to induce cell injury. Fortunately, there is an antioxidan t system that protects organisms against ROS. Indeed, when ROS exceed antioxidant capacity, the resulting cell injury can cause diverse physiological and pathological changes that could lead to a disease like DR. Objective: This paper reviews the possible mechanisms of common and novel biomarkers involved in the development of DR and explores how these biomarkers could be used to monitor the damage induced by oxidative stress in DR, which is a significant complication in people with diabetes. Conclusion: The poor control of glucemy in pacients with DB has been shown contribute to the development of complications in eyes as DR. [ABSTRACT FROM AUTHOR]

Background: Cyclodextrins are active pharmaceutical ingredients to treat neurological diseases by reducing neurotoxicity. The aim of this study was to test if combined consumption of β-cyclodextrin (BCD) and Oleic acid (OA) potentiates brain antioxidant protection. Methods: Four groups of young Wistar rats, grouped in 6 animals each, were treated as follows: Group (G) 1, saline solution 0.9% (control); G2, BCD (0.7 g/kg); G3, OA (15 ml/kg); G4, BCD + OA. The same design was assayed for groups of adult rats. Treatments were daily administered by oral means for five consecutive days. On the last day of administration, brains of the animals were extracted to measure dopamine, 5-HIAA, glutathione (GSH), ATPase, Lipoperoxidation and H2O2. Results: Oleic acid and β-cyclodextrin upgraded the levels of dopamine, 5-HIAA and lipid peroxidation and downgraded the concentrations of GSH and H2O2 in cortex, hemispheres (striatum) and cerebellum/medulla oblongata regions. Conclusions: The results of the present study suggest that combined use of oleic acid and β-cyclodextrin may increase oxidative damage in brain regions and promote alteration in dopamine and 5-HIAA amines and hence, constitutes health risks among age of subjects. [ABSTRACT FROM AUTHOR]