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Neuroprotective effects of a new glutathione peroxidase mimetic on neurons of the chick embryo's retina
Author(s) -
Castagné Vincent,
Clarke Peter G.H.
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(20000215)59:4<497::aid-jnr4>3.0.co;2-b
Subject(s) - neuroprotection , retina , programmed cell death , glutathione peroxidase , axotomy , microbiology and biotechnology , retinal ganglion cell , lipid peroxidation , glutathione , retinal degeneration , biology , ganglion , neuroscience , pharmacology , apoptosis , biochemistry , oxidative stress , regeneration (biology) , enzyme
During their period of naturally occurring neuronal death, retinal ganglion cells are particularly vulnerable to axotomy. The resulting cell death requires protein synthesis and is redox‐regulated, since antioxidants protect axotomized‐ganglion cells when given in doses that maintain the redox status near an optimal set‐point. Here we report the effects of BXT‐51072, a new glutathione peroxidase mimetic, on ganglion cell death induced in various ways in the retinas of chick embryos. The intraocular injection of BXT‐51072 protected axotomized neurons at doses in a narrow (tenfold) range. It also reduced the deleterious effects of intraocular tert‐butyl hydroperoxide, an inducer of lipid peroxidation, and diminished the excitotoxic degeneration induced by N‐methyl‐D‐aspartate. However, BXT‐51072 did not noticeably reduce naturally occurring cell death. Globally, our results show that BXT‐51072 has numerous protective effects in the retina. In accordance with published data, the present report indicates that glutathione peroxidase mimetics may have potential applications for neurologic or degenerative diseases. J. Neurosci. Res. 59:497–503, 2000 © 2000 Wiley‐Liss, Inc.