Epidemiological and toxicological studies indicate a clear negative effect of lead on the central nervous system, and, in particular, the functions and structures of the brain. However, there is still no common understanding of the mechanisms by which these effects are realized at the molecular and cellular levels. Purpose of the study: search, generalization and systematization of materials devoted to the mechanisms of the harmful effects of lead on the nervous system at the molecular and cellular levels.
Materials and methods. The search for publications was carried out using the PubMed, Scopus and RSCI databases, as well as the Russian scientific electronic library CyberLeninka. The selection of articles was carried out on the basis of the presence of information in them about the negative impact of pollutants of various chemical and physical nature on the mitochondrial apparatus. More than 550 articles were identified, resulting in 44 full-text publications being selected.
Results. Most of the described mechanisms of the pathogenesis of lead intoxication have a pronounced dose-dependence of effect both in vivo and in vitro. The neurotoxic effect of lead is realized through any route of entry due to several mechanisms: changes in antioxidant status, replacement of ions of divalent elements by the mechanism of ion mimicry, changes in the structure and functions of intracellular organelles, primarily mitochondria and the endoplasmic reticulum, induction of autophagy, effects on the cell receptor apparatus, changes in synaptic plasticity, effects on the genetic apparatus of the cell.
Conclusion. Understanding the mechanisms of lead neurotoxicity makes it possible to identify “critical points” for the development of methods for early diagnosis of lead-induced pathology of the nervous system and therapeutic and preventive measures.