Oxidative Stress and Neurotoxicity Induced by Lead Exposure: A Comprehensive Review of Molecular Mechanisms and Therapeutic Landscapes

Lead (Pb) exists as a widespread environmental contaminant which creates both immediate and long-term dangers to worldwide public health, especially in relation to neurodevelopment and cognitive abilities. The existence of chronic low-level exposure to lead remains a major medical challenge despite government efforts to control lead pollution in the environment. The research provides a thorough analysis of lead-induced neurotoxicity through its detailed examination of the three processes which involve molecular and cellular and systemic operations while focusing on the creation of oxidative stress. Lead disrupts the delicate intracellular pro-oxidant/antioxidant equilibrium through its power to create reactive oxygen species and reactive nitrogen species while it reduces the body’s natural antioxidant system which includes glutathione and key metalloenzymes which include superoxide dismutase and catalase. We synthesize current literature on how this persistent oxidative stress precipitates mitochondrial dysfunction, induces neuroinflammation via microglial activation, and irreversibly alters synaptic plasticity. The ability of lead to act as a toxic substitute for vital divalent cations which include calcium (Ca^2+) and zinc (Zn^2+) causes major disruptions in neurotransmission by changing glutamatergic N-methyl-D-aspartate (NMDA) receptor signaling and protein kinase C (PKC) pathways.