Selected biochemical mechanisms of lead neurotoxicity

Abstract

Elevated levels of lead ions (Pb²⁺) in the bloodstream present a fatal risk to all age demographics. Furthermore, a wealth of research underscores that chronic exposure to even low, nonsymptomatic doses can trigger developmental disorders in children. Various studies have illustrated the competitive nature of Pb²⁺ with divalent metals from the metabolic pool, notably calcium ions (Ca²⁺). By exploiting transport pathways and binding sites on specific proteins, Pb²⁺ can infiltrate nearly every organ, including the brain. The N-methyl-D-aspartate receptor (NMDAR) is recognized as one of the key molecular targets for Pb²⁺. Mitochondria are also the subject of many studies investigating the toxicity of lead. Maintaining the health of the fragile developing nervous system during prenatal and neonatal stages necessitates diligent monitoring and reassessment of what constitutes safe lead ion concentrations in the bloodstream.