Oxidative stress is an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants. Oxygen byproducts are relatively non-reactive but some of these can undergo metabolism within the biological system to give rise to these highly reactive oxidants. However, free radicals can chemically interact with cell components such as DNA, protein or lipid and steal their electrons in order to become stabilized. This, in turn, destabilizes the cell component molecules which then seek and steal an electron from another molecule, therefore triggering a large chain of free radical reactions 1 Reactive oxygen species (ROS) are produced in many aerobic
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It activates the GLUT4 inward glucose transporter in muscle and fat and promotes phosphorylation of glucose in the liver. The whole body thus stores fats in adipocytes and glycogen in the liver. These stores are maintained and when the muscles require glucose, then the demand can be met through the available short-term glycogen stores. Thus, the excess of glucose is managed well, keeping the plasma glucose concentration near normal. In case of neurons, this condition differs. The glucose is transported to the brain across the blood-brain barrier with the help of GLUTs. The microvessels of the brain express GLUT 1 which is unresponsive to insulin. Thus the brain glucose uptake appears to be insulin independent. Neuron culture studies have shown the glucose uptake to be independent of insulin. The regional distribution of GLUT4 suggests that insulin-dependent glucose uptake might occur in specialized neuronal phenotypes but, in general, vascular barriers offer neurons the only protection against glucose toxicity during hyperglycaemia. GLUT 8 is a newly identified glucose transporter that has also been identified in the brain, localized specifically to the hippocampus, the cerebral cortex and the hypothalamus. Studies of this transporter in the hippocampus suggest that it does not respond to insulin but that it is activated by glucose itself, which recruits GLUT 8 to the plasma membrane. GLUT 8 might represent an insulin-independent glucose-uptake carrier that is specific to certain neurons. Alternatively, it might respond to increases in intracellular
It activates the GLUT4 inward glucose transporter in muscle and fat and promotes phosphorylation of glucose in the liver. The whole body thus stores fats in adipocytes and glycogen in the liver. These stores are maintained and when the muscles require glucose, then the demand can be met through the available short-term glycogen stores. Thus, the excess of glucose is managed well, keeping the plasma glucose concentration near normal. In case of neurons, this condition differs. The glucose is transported to the brain across the blood-brain barrier with the help of GLUTs. The microvessels of the brain express GLUT 1 which is unresponsive to insulin. Thus the brain glucose uptake appears to be insulin independent. Neuron culture studies have shown the glucose uptake to be independent of insulin. The regional distribution of GLUT4 suggests that insulin-dependent glucose uptake might occur in specialized neuronal phenotypes but, in general, vascular barriers offer neurons the only protection against glucose toxicity during hyperglycaemia. GLUT 8 is a newly identified glucose transporter that has also been identified in the brain, localized specifically to the hippocampus, the cerebral cortex and the hypothalamus. Studies of this transporter in the hippocampus suggest that it does not respond to insulin but that it is activated by glucose itself, which recruits GLUT 8 to the plasma membrane. GLUT 8 might represent an insulin-independent glucose-uptake carrier that is specific to certain neurons. Alternatively, it might respond to increases in intracellular