Galactose alters markers of oxidative stress and acetylcholinesterase activity in the cerebrum of rats: protective role of antioxidants

• Published in: Metabolic brain disease Vol. 32; no. 2; pp. 359 - 368
• Main Authors: Delwing-de Lima, Daniela, Fröhlich, Monique, Dalmedico, Leticia, Aurélio, Juliana Gruenwaldt Maia, Delwing-Dal Magro, Débora, Pereira, Eduardo Manoel, Wyse, Angela T.S.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-04-2017; Springer Nature B.V
• Subjects: Acetylcholinesterase - metabolism; alpha-Tocopherol - pharmacology; Animals; Antioxidants - pharmacology; Ascorbic Acid - pharmacology; Biochemistry; Biomedical and Life Sciences; Biomedicine; Catalase - metabolism; Cerebrum - drug effects; Cerebrum - enzymology; Cerebrum - metabolism; Galactose - pharmacology; Glutathione - pharmacology; Glutathione Peroxidase - metabolism; In Vitro Techniques; Male; Metabolic Diseases; Neurology; Neuroprotective Agents - pharmacology; Neurosciences; Oncology; Original Article; Oxidative Stress - drug effects; Protein Carbonylation - drug effects; Rats; Rats, Wistar; Superoxide Dismutase - metabolism; Oxidative stress; Galactose; Antioxidant; Acetylcholinesterase; Cerebrum
• ISSN: 0885-7490; 1573-7365
• DOI: 10.1007/s11011-016-9915-x

We evaluated the
in vitro
effects of galactose at 0.1, 3.0, 5.0 and 10.0 mM on thiobarbituric acid-reactive substances (TBA-RS), total sulfhydryl content, protein carbonyl content, on the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and on acetylcholinesterase (AChE) activity in the cerebral cortex, cerebellum and hippocampus of rats. We also investigated the influence of the antioxidants (each at 1 mM), α-tocopherol, ascorbic acid and glutathione, on the effects elicited by galactose on the parameters tested. Results showed that galactose, at a concentration of 3.0 mM, enhanced TBA-RS levels in the hippocampus, cerebral cortex and cerebellum of rats. In the cerebral cortex, galactose at concentrations of 5.0 and 10.0 mM increased TBA-RS and protein carbonyl content, and at 10.0 mM increased CAT activity and decreased AChE activity. In the cerebellum, galactose at concentrations of 5.0 and 10.0 mM increased TBA-RS, SOD and GSH-Px activities. In the hippocampus, galactose at concentrations of 5.0 and 10.0 mM increased TBA-RS and CAT activity and at 10.0 mM decreased GSH-Px. Data showed that at the pathologically high concentration (greater than 5.0 mM), galactose induces lipid peroxidation, protein carbonylation, alters antioxidant defenses in the cerebrum, and also alters cholinesterase activity. Trolox, ascorbic acid and glutathione addition prevented the majority of alterations in oxidative stress parameters and the decrease in AChE activity that were caused by galactose. Our findings lend support to a potential therapeutic strategy for this condition, which may include the use of appropriate antioxidants for ameliorating the damage caused by galactose.