Bromocriptine prevents neuron damage following inhibition of superoxide dismutase in cultured ventral spinal cord neurons

Abstract

Rpsen et al. have reported point mutations in the cytosolic Cu/Zn superoxide dismutase (SOD 1) gene in some families with familial amyotrophic lateral sclerosis (ALS). To determine whether decreased SOD activity could contribute to neuronal damage, rat embryo ventral spinal cord neurons were incubated with diethyldithiocarbamate (DOC), an inhibitor of SOD. There was a marked increase in neuronal damage in cultures exposed to DOC and this phenomenon was dose-related. In this paradigm, these deteriorative changes were prevented by bromocriptine. DOC-treated ventral spinal cord neurons provide an in vitro model of free radical neurotoxicity secondary to decreased SOD activity. Simultaneous treatment with bromocriptine and DOC reduced neurotoxicity, indicating that bromocriptine has a neuroprotective effect against free radicals. Neural Res 1997; 19: 389-392]