MITOCHONDRIAL INDUCTION OF ADULT T-CELL LEUKEMIA-DERIVED FACTOR (ADF HTX) AFTER OXIDATIVE STRESSES IN RETINAL-PIGMENT EPITHELIAL-CELLS/

Citation
Cd. Gauntt et al., MITOCHONDRIAL INDUCTION OF ADULT T-CELL LEUKEMIA-DERIVED FACTOR (ADF HTX) AFTER OXIDATIVE STRESSES IN RETINAL-PIGMENT EPITHELIAL-CELLS/, Investigative ophthalmology & visual science, 35(7), 1994, pp. 2916-2923
Citations number
53
Categorie Soggetti
Ophthalmology
ISSN journal
01460404
Volume
35
Issue
7
Year of publication
1994
Pages
2916 - 2923
Database
ISI
SICI code
0146-0404(1994)35:7<2916:MIOATL>2.0.ZU;2-P
Abstract
Purpose. Adult T cell leukemia derived factor (ADF) is a human homolog ue of thioredoxin (hTx), which exhibits scavenging activity with react ive oxygen intermediates. In their previous study, the authors found t hat after transient retinal ischemia, the expression of thioredoxin in rat retinal pigment epithelium (RPE) layer increased markedly. The pr esent investigation is to determine intracellular ADF localization in RPE after transient ischemia and in cultured human RPE cells after oxi dative insult by H2O2. Methods. The authors employed immunoelectron mi croscopy to examine ADF localization in RPE. Labeling density analysis was performed to supplement the main observation in the experiment of transient retinal ischemia. -(4,5-dimethylthiazol-2yl)-2-5-diphenylte trazolium bromide (MTT) assay was performed to verify the protective r ole of recombinant ADF (rADF) against H2O2. Results. In immunogold ele ctron microscopy, sparse ADF-positive labeling was seen in the cytosol and mitochondria in normal rat RPE and in untreated cultured RPE cell s. After oxidative stress, it was concentrated in mitochondria in both groups. MTT assay proved that rADF protected cultured RPE from the to xicity of H2O2. Conclusions. This study shows the induction of ADF/hTx in mitochondria of RPE after oxidative stresses and its protective ef fect on cultured RPE exposed to H2O2. The data indicate the possibly i mportant role of ADF/hTx in the protection of retinal cells from the o xidative stresses associated with retinal ischemic disease and probabl y with regular visual activity.