In:
Human & Experimental Toxicology, SAGE Publications, Vol. 27, No. 4 ( 2008-04), p. 327-339
Abstract:
Siderosis bulbi is vision threatening. An investigation into its mechanisms and management is crucial. Experimental siderosis was established by intravitreous administration of an iron particle (chronic) or FeSO 4 (acute). After siderosis, there was a significant dose-responsive reduction in eletroretinogram (a/b-wave) amplitude, and an increase in • OH level, greater when caused by 24 mM FeSO 4 than that by 8 mM FeSO 4 . Furthermore, the FeSO 4 -induced oxidative stress was significantly blunted by 100 μM ferulic acid (FA). Siderosis also resulted in an excessive glutamate release, increased [Ca ++ ] i , and enhanced superoxide dismutase immunoreactivity. The latter finding was consistent with the Western blot result. Obvious disorganization including loss of photoreceptor outer segments and cholinergic amacrines together with a wide-spreading ferric distribution across the retina was present, which were related to the eletro-retinographic and pathologic dysfunctions. Furthermore, b-wave reduction and amacrine damage were respectively, significantly, dose-dependently, and clearly ameliorated by FA. Thus, siderosis stimulates oxidative stress, and possibly, subsequent excitotoxicity, and calcium influx, which explains why the retina is impaired electro-physiologically and pathologically. Importantly, FA protects iron toxicity perhaps by acting as a free radical scavenger. This provides an approach to the study and treatment of the iron-related disorders such as retained intraocular iron and Alzheimer disease.
Type of Medium:
Online Resource
ISSN:
0960-3271
,
1477-0903
DOI:
10.1177/0960327108092294
Language:
English
Publisher:
SAGE Publications
Publication Date:
2008
detail.hit.zdb_id:
1483723-7
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