%0 Journal Article
%T Myosins Are Differentially Expressed under Oxidative Stress in Chronic Streptozotocin-Induced Diabetic Rat Brains
%A Luciana Karen Cal¨˘bria
%A Alice Vieira da Costa
%A Renato Jos¨¦ da Silva Oliveira
%A Simone Ramos Deconte
%A Rafael Nascimento
%A Washington JoŁżo de Carvalho
%A Vanessa Neves de Oliveira
%A Carlos Alberto Arcaro Filho
%A Luciana Rezende Alves de Oliveira
%A Luiz Ricardo Goulart
%A Foued Salmen Espindola
%J ISRN Neuroscience
%D 2013
%R 10.1155/2013/423931
%X Diabetes mellitus is a disease characterized by persistent hyperglycemia, which may lead to brain tissue damage due to oxidative stress and also contributes to neuronal death and changes in synaptic transmission. This study evaluated the effect of oxidative stress and the use of antioxidants supplementation on myosins expression levels in the brains of chronic diabetic rats induced by streptozotocin. Lipid peroxidation, antioxidant enzymes activities, and myosins-IIB and -Va expressions at transcriptional and translational levels were examined after 90 days induction. The chronic effect of the diabetes led to the upregulation of superoxide dismutase (SOD) and catalase (CAT) activities, and the downregulation of glutathione peroxidase (GPx), but there was no statistically significant increase in the malondialdehyde (MDA) levels. These alterations were accompanied by high myosin-IIB and low myosin-Va expressions. Although the antioxidant supplementation did not interfere on MDA levels, the oxidative stress caused by chronic hyperglycemia was reduced by increasing SOD and restoring CAT and GPx activities. Interestingly, after supplementation, diabetic rats recovered only myosin-Va protein levels, without interfering on myosins mRNA levels expressed in diabetic rat brains. Our results suggest that antioxidant supplementation reduces oxidative stress and also regulates the myosins protein expression, which should be beneficial to individuals with diabetes/chronic hyperglycemia. 1. Introduction Diabetes mellitus is a multifactorial disease characterized by chronic hyperglycemia resulting from abnormalities in insulin action and/or insulin secretion [1]. Research evidences support that both acute and chronic hyperglycemia produce negative impacts on the central nervous system leading to tissues damage [2, 3]. One mechanism behind this neuronal injury is oxidative stress, due to the excessive free radical generation from the oxidation of elevated intracellular glucose levels [4]. The brain contains large amounts of enzymes to protect against oxidative damage [5]. Endogenous antioxidant system, including enzymatic (glutathione peroxidase, superoxide dismutase, and catalase) and nonenzymatic (vitamin E, vitamin C, glutathione, and uric acid) antioxidants, offers protection to cells and tissues against glucose-induced oxidative injury in diabetics [6¨C10]. The enhancement on oxygen free radical in brain during hyperglycemia [11] contributes to increased neuronal death trough protein oxidation, DNA damage, and peroxidation of membrane lipids [12] as well as changes
%U http://www.hindawi.com/journals/isrn.neuroscience/2013/423931/