The destructive pathologic and biochemical consequences of methyl merc
ury have been extensively described. Relatively little is known, howev
er, about the defensive mechanisms neurons employ to protect themselve
s against mercurial injury. Studies using a variety of cell types have
disclosed several inducible biochemical responses to heavy metal and
pro-oxidant insult These responses include modulation of cellular leve
ls of glutathione, metallothionein, hemoxygenase, and other stress pro
teins. With few exceptions, however, neurons appear to be markedly def
icient in these responses. This suggests the possibility that the phen
omenon of selective vulnerability of cells in the nervous system to me
rcury and other heavy metals may arise from a critical absence of inhe
rent protective mechanisms. Transfection of neural cells with the anti
-apoptotic gene, bcl-2, confers partial resistance to a variety of neu
rotoxins, including methyl mercury. This approach to providing neuropr
otection may represent an efficacious strategy for combating tenacious
neurotoxins such as methyl mercury. 1996 Intox Press, Inc.