A 1998 article suggested that ebselen might be a good neuroprotective drug. Your doctor needs to reconcile the deleterious contradictions between these 2 articles.
http://online.liebertpub.com/doi/abs/10.1089/dna.2012.1939
ABSTRACT
The
seleno-organic compound and radical scavenger ebselen
(2-phenyl-1,2-benzisoselenazol-3(2H)-one) have been extensively employed
as an anti-inflammatory and neuroprotective compound. However, its
glutathione peroxidase activity at the expense of cellular thiols groups
could underlie certain deleterious actions of the compound on cell
physiology. In this study, we have analyzed the effect of ebselen on rat
hippocampal astrocytes in culture. Cellular viability, the
intracellular free-Ca2+ concentration ([Ca2+]c), the mitochondrial free-Ca2+ concentration ([Ca2+]m), and mitochondrial membrane potential (ψm)
were analyzed. The caspase-3 activity was also assayed. Our results
show that cell viability was reduced by treatment of cells with ebselen,
depending on the concentration employed. In the presence of ebselen, we
observed an initial transient increase in [Ca2+]c that was then followed by a progressive increase to an elevated plateau. We also observed a transient increase in [Ca2+]m in the presence of ebselen that returned toward a value over the prestimulation level. The compound induced depolarization of ψm
and altered the permeability of the mitochondrial membrane.
Additionally, a disruption of the mitochondrial network was observed.
Finally, we did not detect changes in caspase-3 activation in response
to ebselen treatment. Collectively, these data support the likelihood of
ebselen, depending on the concentration employed, reduces viability of
rat hippocampal astrocytes via its action on the mitochondrial activity.
These may be early effects that do not involve caspase-3 activation. We
conclude that, depending on the concentration used, ebselen might exert
deleterious actions on astrocyte physiology that could compromise cell
function.
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