Gene interactions and pathways from curated databases and text-mining
FASEB J 2003, PMID: 12424220

Selenium deficiency increases susceptibility to glutamate-induced excitotoxicity.

Savaskan, Nicolai E; Bräuer, Anja U; Kühbacher, Markus; Eyüpoglu, Ilker Y; Kyriakopoulos, Antonios; Ninnemann, Olaf; Behne, Dietrich; Nitsch, Robert

Excitotoxic brain lesions, such as stroke and epilepsy, lead to increasing destruction of neurons hours after the insult. The deadly cascade of events involves detrimental actions by free radicals and the activation of proapoptotic transcription factors, which finally result in neuronal destruction. Here, we provide direct evidence that the nutritionally essential trace element selenium has a pivotal role in neuronal susceptibility to excitotoxic lesions. First, we observed in neuronal cell cultures that addition of selenium in the form of selenite within the physiological range protects against excitotoxic insults and even attenuates primary damage. The neuroprotective effect of selenium is not directly mediated via antioxidative effects of selenite but requires de novo protein synthesis. Gel shift analysis demonstrates that this effect is connected to the inhibition of glutamate-induced NF-kappaB and AP-1 activation. Furthermore, we provide evidence that selenium deficiency in vivo results in a massive increase in susceptibility to kainate-induced seizures and cell loss. These findings indicate the importance of selenium for prevention and therapy of excitotoxic brain damage.

Diseases/Pathways annotated by Medline MESH: Disease Susceptibility, Neurotoxicity Syndromes, Seizures
Document information provided by NCBI PubMed

Text Mining Data

AP-1 → NF-kappaB: " Gel shift analysis demonstrates that this effect is connected to the inhibition of glutamate induced NF-kappaB and AP-1 activation "

Manually curated Databases

No curated data.