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Science Forum Index » Life Extension Forum » Selenium effectively inhibits ROS-mediated apoptotic...
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 Posted: Wed May 14, 2008 11:42 am |
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Sodium selenite is not the form in selenium yeast but it looks like it
may in effect be doing the same thing i.e., its role as an antioxidant
cofactor.
Biochim Biophys Acta. 2007 Dec;1772(11-12):1199-210. Epub 2007 Sep 29.
Links
Yeo JE, Kang SK.
Department of Physiology, School of Medicine, Pusan National
University, 1-10, Ami-Dong, Seo-Gu, Busan, 602-739, South Korea.
This study was designed to investigate possible prevention of
apoptotic cell death by selenium, an antioxidant, using cultured brain-
derived neural progenitor cells (NPCs) and an experimental mouse brain
trauma (BT) model. We tested some of the neuroprotective effects of
sodium selenite in NPC cells by monitoring thioredoxin reductase (TR)
expression, optimum H(2)O(2) removal, and consequent inhibition of pro-
apoptotic events including cytochrome c release and caspase 3 and 9
activation. Analysis of key apoptotic regulators during H(2)O(2)-
induced apoptosis of NPCs showed that selenite blocks the activation
of c-jun N-terminal protein kinase (JNK)/P38 mitogen-activated protein
kinase (MAPK), and Akt survival protein. Moreover, selenite activates
p44/42 MAPK and inhibits the downregulation of Bcl2 in selenite-
treated NPC cells. For in vivo experiments, the effects of selenite on
H(2)O(2) neurotoxicity were tested using several biochemical and
morphologic markers. Here we show that selenite potentially inhibits
H(2)O(2)-induced apoptosis of NPCs and in traumatic brain injury. This
in vivo protective function was also associated with inhibition of
H(2)O(2)-induced reactive oxygen species (ROS) generation, cytochrome
c release and caspase 3 and 9 activation. Our data show that the
protective function of selenite through attenuation of secondary
pathological events most likely results from its comprehensive effects
that block apoptotic cell death, resulting in the maintenance of
functional neurons and in inhibition of astrogliosis. The finding that
selenite administration prevents secondary pathological events in an
animal model of traumatic brain injury, as well as its efficacy, may
provide novel drug targets for treating brain trauma.
PMID: 17997286 [PubMed - indexed for MEDLINE] |
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