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Lead-calcium interactions in cellular lead toxicity.

The interaction of Pb and Ca with cellular sites depends upon the concentration of free ions present (Pb2+, Ca2+). The ability of Pb2+ to form complexes with simple anions such as Cl- and OH-, the formation of precipitates such as Pb(OH)2 and Pb3(PO4)2, and the ubiquity of Pb as a contaminant in laboratory reagents implies that particular care is needed in order to define the Pb2+ concentration of a solution. The free Pb2+ concentration may be controlled with Pb2+ buffers, and measured with a Pb2+ selective electrode, a fluorescent dye, fura-2, or an NMR indicator, 19F-BAPTA. Pb(2+)-Ca2+ interactions occur in three main situations at the cellular level. Pb2+ and Ca2+ compete at the plasma membrane for transport systems which effect their entry or exit, such as Ca2+ channels, and the Ca2+ pump. Intracellular Ca2+ is buffered to around 10(-7) M by proteins, endoplasmic reticulum and mitochondria. Pb2+ disturbs intracellular Ca2+ homeostasis. Ca(2+)-Pb2+ interactions at mitochondria have been described, but other mechanisms have not yet been explored. Increases in intracellular [Ca2+] act as a signal (or second messenger). Pb2+ interacts with a number of Ca(2+)-dependent effector mechanisms, such as calmodulin (a Ca2+ receptor protein which couples to several enzymes e.g., phosphodiesterase, protein kinases), protein kinase C, Ca(2+)-dependent K+ channels in the plasma membrane and neurotransmitter release. The actions of Pb2+ on neurotransmission may be relevant to Pb(2+)-induced human neuropathy and encephalopathy.