Sulforaphane is anticonvulsant and improves mitochondrial function

Carrasco-Pozo, Catalina, Tan, Kah Ni and Borges, Karin (2015) Sulforaphane is anticonvulsant and improves mitochondrial function. Journal of Neurochemistry, 135 5: 932-942. doi:10.1111/jnc.13361

Author Carrasco-Pozo, Catalina
Tan, Kah Ni
Borges, Karin
Title Sulforaphane is anticonvulsant and improves mitochondrial function
Journal name Journal of Neurochemistry   Check publisher's open access policy
ISSN 0022-3042
Publication date 2015-12-01
Year available 2015
Sub-type Article (original research)
DOI 10.1111/jnc.13361
Open Access Status Not Open Access
Volume 135
Issue 5
Start page 932
End page 942
Total pages 11
Place of publication Chichester, West Sussex, United Kingdom
Publisher Wiley-Blackwell Publishing
Language eng
Abstract The nuclear factor erythroid 2-related factor 2 pathway (Nrf2) has been previously identified to protect the brain against various impacts. Here, we investigated the effect of the Nrf2 activator sulforaphane in various seizure models and hippocampal mitochondrial bioenergetics. We found that daily injections of sulforaphane for 5 days elevated the seizure thresholds to 6 Hz stimulation and fluorothyl-, but not pentylenetetrazole-induced tonic seizures and protected mice against pilocarpine-induced status epilepticus (SE). Also, sulforaphane increased the antioxidant defences within hippocampal formations and blood plasma. In addition, sulforaphane treatment reduced the extent of hippocampal lipid peroxidation 24 h post-SE and protected hippocampal mitochondria against SE-induced reduction in state 2 and uncoupler-stimulated state 3 respiration. SE-mediated partial loss of rotenone-sensitive and complex II-driven respiration was reduced, consistent with the enhanced activities of complexes I and II in sulforaphane-treated SE mice. In mitochondria isolated from both no SE and SE mice, sulforaphane increased state 3 respiration and respiration linked to ATP synthesis, which may contribute to its anticonvulsant and antioxidant effects by providing more ATP for cellular vital and protective functions. However, sulforaphane did not prevent SE-induced hippocampal cell death. In conclusion, sulforaphane and/or Nrf2 activation are viable anticonvulsant strategies, which are antioxidant and enhance mitochondrial function, especially the ability to produce ATP.
Keyword Epilepsy
Mitochondrial respiration
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID 1044407
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2016 Collection
School of Biomedical Sciences Publications
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 15 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 16 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Sun, 24 Jan 2016, 10:17:23 EST by System User on behalf of Learning and Research Services (UQ Library)