REVIEW PAPER
Role of Zinc in nervous system cells
 
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Independent Laboratory for Cell Metabolism, Institute of Rural Health, Lublin, Poland
 
 
J Pre Clin Clin Res. 2011;5(1):12-15
 
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ABSTRACT
Zinc has been identified as one of the most important minerals in the human body. As a trace element, zinc (Zn) is vital for the growth and development of an organism. Its basic functioning centres around its involvement in the structure of macro-elementary compounds, and the activation of numerous enzymes engaged in the metabolic processes. In the organic world, over 300 zinc-dependent enzymes have been identified. Our bodies need zinc to make insulin and eliminate toxins, and zinc is also important for the anti-oxidant maintenance and maintaining a healthy immune system. Laboratory experiments appeared discharged its ant-oxidant functions. The first is that dozens of vital enzymes within the body contain zinc, and in these enzymes the zinc molecule acts directly as an anti-oxidant, protecting the biochemical structure of the enzyme from free radical attack. Secondly, zinc acts to stabilize protein which may otherwise react with highly unstable minerals, particularly iron and copper, to form free radicals. Furthermore, zinc plays a very important role in normal brain development and function. In growing organisms, zinc is known to be indispensable for the undisturbed formation of their nervous systems. In adults, zinc deficiency results in behavioral symptoms, such as memory problems, malaise, or higher susceptibility to stress. On the other hand, it is believed that an excess of free zinc is detrimental and can lead to neuronal death. Studies confirm that the toxicity of zinc shows up when there is an increase in the third fraction or free zinc in a cell (pool of zinc, so called ‘free” zinc, which is not bound to proteins). The neurotoxicity of zinc has been demonstrated on animal models in which a stroke, ischemia, Alzheimer’s disease, or convulsions were induced. The detailed mechanism of the toxic activity of zinc is not known, but it seems that the main cause of neuronal death is low energy production by mitochondria.
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