Heavy metals modulate glutamatergic system in human platelets

Research strategies have been developed to characterize parameters in peripheral tissues that might easily be measured in humans as surrogate markers of damage, dysfunction or interactions involving neural targets of toxicants. The similarities between platelet and neuron may even be clinically important, as a number of biochemical markers show parallel changes in the central nervous system (CNS) and platelets. The purpose of our research was to investigate the effect of Hg2+, Pb2+ and Cd2+ on the [H-3]-glutamate binding and [H-3]-glutamate uptake in human platelets. The involvement of oxidative stress in the modulation of glutamatergic system induced by heavy metals was also investigated. The present study clearly demonstrates that Hg2+, Cd2+, and Pb2+ inhibited [H-3]-glutamate uptake in human platelets. Hg2+ inhibited [H-3]-glutamate binding, while Cd2+ and Pb2+ stimulated [H-3]-glutamate binding in human platelets. Hg2+, Cd2+ and Pb2+ increased lipid peroxidation levels and reactive oxygen species (ROS) measurement in platelets. The present limited results could suggest that glutamatergic system may be used as a potential biomarker for neurotoxic action of heavy metals in humans.