OXIDATIVE STRESS INDUCES ADULT T-CELL LEUKEMIA-DERIVED FACTOR THIOREDOXIN IN THE RAT RETINA

Citation
A. Ohira et al., OXIDATIVE STRESS INDUCES ADULT T-CELL LEUKEMIA-DERIVED FACTOR THIOREDOXIN IN THE RAT RETINA, Laboratory investigation, 70(2), 1994, pp. 279-285
Citations number
31
Categorie Soggetti
Pathology,"Medicine, Research & Experimental
Journal title
ISSN journal
00236837
Volume
70
Issue
2
Year of publication
1994
Pages
279 - 285
Database
ISI
SICI code
0023-6837(1994)70:2<279:OSIATL>2.0.ZU;2-U
Abstract
BACKGROUND: Adult T cell leukemia derived factor (ADF), originally def ined as an interleukin-2 receptor inducer, is a human thioredoxin homo log. ADF/thioredoxin has several biologic functions, such as defense a gainst cellular damage, activity to scavenge oxidative stress by hydro gen peroxide radicals and cytokine-like properties. We hypothesized th at under certain conditions, ischemia followed by reperfusion and/or l ight exposure, ADF may be induced in the retina.EXPERIMENTAL DESIGN: T o test this hypothesis, we prepared experimental animal models in whic h oxidative stress could be applied to the retina. In the present stud y, we examined ADF expression in the rat retina using temporary ischem ia and reperfusion, and photodynamic retinal vascular thrombosis by im munohistochemical and Western blotting methods. RESULTS: ADF expressio n was strongly induced in the retinal pigment epithelial cells after 2 hours of ischemia followed by 2, 24, or 48 hours of reperfusion. ADF was also expressed in retinal pigment epithelial cells as early as 3 h ours after light exposure followed by rose bengal injection, and this expression increased with time. Western blotting data showed that ADF expression increased in the retinal pigment epithelial cells in the ex perimental group, as compared with the control group. These results in dicate that ADF is actively induced in retinal pigment epithelial cell s upon oxidative stress. CONCLUSIONS: ADF induction in retinal pigment epithelial cells may be involved in the defense mechanism against cel lular damage caused by active oxygen species generated during oxygen s tress to the retina.