Immunohistochemical localization of neuronal and glial calcium-binding proteins in hippocampus of chronically low level lead exposed rhesus monkeys.

: The purpose of this study was to investigate the distribution of the neuronal calcium-binding proteins parvalbumin, calbindin D28k, calretinin and the glial protein S100 in the hippocampus of lead exposed rhesus monkeys. It has been suggested that lead may exert its toxic effects by perturbing the intracellular calcium homeostasis. Lead is able to increase the intracellular Ca2+ concentration and can serve as a calcium substitute. It has been shown that some calcium-binding proteins are capable of binding lead. We tried to find a putative dose-depending relation between long-term low level lead exposure and the expression of the proteins investigated. Rhesus monkeys were pre- and postnatally exposed to 600 mg-350 mg-0 mg lead-acetate in diet for nine years, as described by Lilienthal et al. (1986). After a lead-free period of 32 months animals were sacrificed. Hippocampal paraffin sections were stained for parvalbumin (PV), calbindin D28k (CB), calretinin (CR), and S100 with immunohistochemical methods. The distribution of the neuronal calcium-binding proteins was almost identical for the different exposure groups. The most striking observation was a marked decrease of S100 immunoreactivity in astrocytes in the high lead group. Considering a protective role against high Ca2+ concentration and Pb2+ accumulation respectively the unchanged expression of PV, CB, and CR remains to be clarified. The apparent difference in S100 expression supports the hypothesis that glial cells are the main target of lead toxicity. The reduced expression may indicate a developmental retardation of astroglia.