Skip to content
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types
Neurochemical Research, Volume 37, No. 1, Year 2012
Notification
URL copied to clipboard!
Description
Metal homeostasis is increasingly being evaluated as a therapeutic target in stroke and neurodegenerative diseases. Metal dysregulation has been shown to lead to protein aggregation, plaque formation and neuronal death. In 2007, we first reported that voltage-gated calcium channels act as a facile conduit for the entry of free ferrous (Fe 2+) ions into neurons. Herein, we evaluate differential iron toxicity to central nervous system cells and assess the ability of the typical L-type voltage-gated calcium channel blocker nimodipine to attenuate iron-induced toxicity. The data demonstrate that iron sulfate induces a dose-dependent decrease in cell viability in rat brain endothelial cells (RBE4; LC 50 = 150 μM), neuronal cells (Neuro-2α neuroblastoma; LC 50 = 400 μM), and in astrocytes (DI TNC1; LC 50 = 1.1 mM). Pre-treatment with nimodipine prior to iron sulfate exposure provided a significant (P < 0.05) increase in viable cell numbers for RBE4 (2.5-fold), Neuro2-α (~2-fold), and nearly abolished toxicity in primary neurons. Astrocytes were highly resistant to iron toxicity compared to the other cell types tested and nimodipine had no (P > 0.05) protective effect in these cells. The data demonstrate variable susceptibility to iron overload conditions in different cell types of the brain and suggest that typical L-type voltage-gated calcium channel blockers (here represented by nimodipine), may serve as protective agents in conditions involving iron overload, particularly in cell types highly susceptible to iron toxicity. © 2011 Springer Science+Business Media, LLC.
Authors & Co-Authors
Lockman, Julie A.
United States, Amarillo
Texas Tech University Health Sciences Center at Amarillo
Geldenhuys, Werner J.
United States, Rootstown
Northeast Ohio Medical University Neomed
Bohn, Kaci A.
United States, Amarillo
Texas Tech University Health Sciences Center at Amarillo
Allen, David D.
United States, Rootstown
Northeast Ohio Medical University Neomed
van der Schyf, Cornelis J.
United States, Rootstown
Northeast Ohio Medical University Neomed
Statistics
Citations: 18
Authors: 5
Affiliations: 2
Identifiers
Doi:
10.1007/s11064-011-0591-2
ISSN:
15736903
Research Areas
Noncommunicable Diseases