Abstract:
:This study investigates the implication of mitochondria- and caspase-dependent pathways in the death of retinal neurones exposed to the neurosteroid pregnenolone sulfate (PS) shown to evoke apoptosis and contribute to amplification and propagation of excitotoxicity. After a brief PS challenge of intact retinas, caspase-3 and caspase-2 activation and cytochrome c release occur early and independent of changes in the oxidative state measured by superoxide dismutase activity. The temporal and spatial relationship of these events suggests that a caspase-3-dependent pathway is activated in response to cytochrome c release and requires caspase-2 activation and a late cytochrome c release in specific cellular subsets of retinal layers. The protection by caspase inhibitors indicates a predominant role of the pathway in PS-induced retinal apoptosis, although a limited use of caspase inhibitors is upheld on a conceivable shift from apoptosis toward necrosis. Conversely, 3alpha-hydroxy-5beta-pregnan-20-one sulfate and 17beta-oestradiol provide complete prevention of PS-induced retinal death.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Cascio C,Guarneri R,Russo D,De Leo G,Guarneri M,Piccoli F,Guarneri Pdoi
10.1046/j.1471-4159.2002.01229.xkeywords:
subject
Has Abstractpub_date
2002-12-01 00:00:00pages
1358-71issue
6eissn
0022-3042issn
1471-4159pii
1229journal_volume
83pub_type
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