Lead markedly amplified L-glutamate-induced oxidative stress, that is,
increased L-glutamate-induced production of reactive oxygen species,
decreased cellular glutathione, and induced cytotoxicity in human neur
oblastoma cells. It was notable that oxidative burst induced by L-glut
amate alone was observed only when neuronal glutathione was depleted.
A role of protein kinase C (PKC) in glutamate-induced production of re
active oxygen species is likely because it was blocked by a PE;C inhib
itor. We suggest here that, the mechanism whereby lead causes its neur
otoxicity may be through the amplification of glutamate-induced oxidat
ive stress, possibly through PKC activation.