Metal Ion Neurotoxicity—Role of Pro-inflammatory Mediators
摘要
Most of the population is affected by neurotoxic metal exposure, which includes aluminium, arsenic, cadmium, lead, manganese, mercury, nitric oxide, cobalt, copper, calcium, lithium, iron, nickel, bismuth, selenium, and zinc. The aberrant functioning of the nervous system as a result of exposure to hazardous substances is known as neurotoxicity (neurotoxicants). Neurotoxicants can cause harm or even death to neurons, which are essential for the brain and other parts of the nervous system to receive and process information. The maintenance of normal physiological functions in the brain is contingent upon the equilibrium of metal ions. Numerous neurological disorders, including neurodegeneration and neurodevelopmental abnormalities, are known to be associated with altered essential metal homeostasis and increased environmental/occupational exposure to xenobiotic metals. Neurotoxicity is frequently caused by an excess of metals in the body. However, neurons produce a variety of cytokines and chemokines that control synaptic activity and act as a cellular and molecular coordinator of neurons’ communication. The study of neurons in brains from various cellular and molecular decades strongly suggests that microglia has a major part in mediating the progressive neurodegenerative process by producing pro-inflammatory and neurotoxic chemicals. In this article, we want to discuss the importance of various metals in the neurotoxicity. This article will also highlight the neurotoxic (inflammation) and neuroprotective (neuroregulatory) role of cytokines and chemokine in the nervous system.