HEAVY METAL-INDUCED NEUROTOXICITY AND IT'S AMELIORATION: ROLE OF GLIAL CELLS

Heavy metal neurotoxicity is a public health concern due to the widespread contamination of arsenic in the environment. Arsenic has been linked to various neurological disorders, ranging from cognitive impairments to neurodegenerative diseases. Glial cells, including astrocytes and microglia, have emerged as key players in mediating the toxic effects of these metals on the central nervous system. This abstract presents a comprehensive overview of the neurotoxicity associated with arsenic, with a specific focus on the role of glial cells. Arsenic-induced reactive astrogliosis and microglial activation lead to the release of pro-inflammatory cytokines and oxidative stress, contributing to neuronal damage. Arsenic also disrupts glial cell maturation and function, impairing their ability to support neuronal survival and synaptic plasticity. Furthermore, the abstract highlights potential strategies for mitigating the neurotoxic effects of these heavy metals, emphasizing the targeting of glial cells. Modulation of glial activation and the subsequent inflammatory response through pharmacological interventions or nutraceutical agents shows promise in ameliorating metal-induced neurotoxicity. Additionally, enhancing the antioxidant defense mechanisms within glial cells represents another potential therapeutic approach. In summary, understanding the involvement of glial cells in the neurotoxic effects of arsenic provides valuable insights into the pathogenesis of metal-induced neurotoxicity. Targeting glial cell function and associated inflammatory processes holds potential for developing novel therapeutic strategies to alleviate heavy metal-induced neurotoxicity and preserve brain health. Further research is needed to unravel the intricate interplay between glial cells and heavy metal toxicity, paving the way for effective preventive and therapeutic interventions. None