Prevention of Oxidative Stress by Omega-3 Fatty Acids in the Brain
Oxidative stress and inflammation are the major mechanisms that contribute to the pathogenesis of neurotraumatic, neurodegenerative, and neuropsychiatric diseases. Two major families of essential fatty acids (omega-6 family and omega-3 family) are known t
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Akhlaq A. Farooqui and Tahira Farooqui
Introduction Neural membranes contain glycerophospholipids, which contain a saturated fatty acid at the sn-1 position of glycerol moiety, whereas the sn-2 position bears a polyunsaturated fatty acid (arachidonic acid, ARA, 20:4, n-6) or docosahexaenoic acid, DHA (22:6, n-3). ARA belongs to the omega-6 family whereas DHA falls under the omega-3 family of essential fatty acids, respectively. Vegetable and fish oils are the most common sources of omega-6 and omega-3 fatty acids, respectively. Fatty acids belonging to omega-6 and omega-3 family not only provide neural membranes with their physical characteristics, such as acyl chain order and fluidity, stability, phase behavior, elastic compressibility, ion permeability, fusion, rapid flip-flop and packing [1], but also function as signaling molecules by supplying lipid mediators, which are formed by the oxidation process. An appropriate ratio of ARA to DHA in the brain promotes development, ameliorates cognitive functions, and provides protection against neurological diseases by enhancing repairing processes [1]. In addition, ARA and DHA also stimulate gene expression, boost synaptogenesis, neurogenesis, and induce and prevent oxidative stress, a process that results from an unbalance between prooxidant and antioxidant systems in the brain. Neurological oxidative stress is either induced by the failure of cell antioxidant (buffering) mechanisms or overproduction of reactive oxygen species (ROS), which are oxygen-based radicals formed in most mammalian cells through the activities of enzymes involved in the mitochondrial electron transport chain, epoxygenase (EPOX), lipoxygenase (LOX) or cyclooxygenase (COX), NAD(P)H oxidases A.A. Farooqui (&) T. Farooqui Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, OH 43210, USA e-mail: [email protected] T. Farooqui e-mail: [email protected] A.A. Farooqui 3120 Herrick Road, Columbus, OH 43221, USA
or uncoupled nitric oxide synthase (NOS), and peroxidases, among others [2, 3]. They are normal by-products of healthy cellular metabolic processes and are known to play physiologically useful roles in cell signaling; for example, as part of the immunity-oriented “oxidative burst” [4]. Low levels of oxidative stress are needed for cell functions. The role of oxygen in cell survival is linked to its high redox potential, which makes it an excellent oxidizing agent capable of accepting electrons easily from reduced substrates. High levels of oxidative stress are central disruptor of neural cell homeostasis. It is well known that brain represents only *2 % of the total body mass and yet accounts for more than 25 % glucose and 20 % of the total consumption of oxygen [5]. In addition to high oxygen utilization, two more reasons make the brain most susceptible to oxidative damage. First is its modest antioxidant defense mechanism and second is the presence of high levels of lipids, which account for 60–65 % of brain dry weight. Thus, the brain is particularl
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