[Physiopathology of inorganic lead poisoning]

This paper gives an overview of the hypotheses concerning the mechanisms of inorganic lead toxicity on cells and tissues, with emphasis on the effect of low-concentration lead. Inhibition of heme synthesis is responsible not only for lead-induced anaemia, but also for accumulation of delta-aminolaevulinic acid (ALA) and for lowering the concentration of cytochromes contained in the mitochondrial respiratory chain. Auto-oxidation of ALA is thought to result in the formation of free radicals. On the other hand, lead replaces ionic calcium in its role as second cell messenger. This mechanism would explain the abnormalities observed in synaptic transmission, arteriolar vasoreactivity and functioning of such cells as osteoclasts and osteoblasts. Nuclear toxicity, with abnormal expression of DNA genes and inhibition of certain enzymes such as membrane Na+/K+ ATPase, are also considered. The mechanisms of tissue toxicity are discussed.