Purchase this article with an account.
Hiroto Shibuki, Naomichi Katai, Junji Yodoi, Koji Uchida, Nagahisa Yoshimura; Lipid Peroxidation and Peroxynitrite in Retinal Ischemia–Reperfusion Injury. Invest. Ophthalmol. Vis. Sci. 2000;41(11):3607-3614.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. To investigate whether lipid peroxides play a role in retinal cell
death due to ischemia–reperfusion injury, whether recombinant human
thioredoxin (rhTRX) treatment reduces production of lipid peroxides of
the retina, and whether such treatment reduces the number of cells
expressing c-Jun and cyclin D1.
methods. Retinal ischemia was induced in rats by increasing the intraocular
pressure to 110 mm Hg for 60 minutes. After reperfusion,
immunohistochemical staining for lipid peroxide, peroxynitrite, c-Jun,
and cyclin D1 and propidium iodide (PI) staining were performed on
retinal sections from animals treated intravenously with and without
rhTRX, a free radical scavenger. Quantitative analyses of PI-, c-Jun-,
and cyclin D1–positive cells were performed after the ischemic insult.
Concentration of lipid peroxides in the retina was determined by the
thiobarbituric acid assay.
results. Specific immunostaining for lipid peroxides was seen in the ganglion
cell layer at 6 hours after reperfusion, in the inner nuclear layer at
12 hours, and in the outer nuclear layer at 48 hours. Time course
studies for PI-positive cells in the three nuclear layers coincided
with those of specific immunostaining for lipid peroxides. The specific
immunostaining was weakened by pre- and posttreatment with 0.5 mg of
rhTRX. The number of PI-, c-Jun-, and cyclin D1–positive cells and the
concentration of lipid peroxides were significantly decreased by
treatment with rhTRX compared with those of vehicle-treated control
rats (P < 0.01).
conclusions. Lipid peroxides formed by free radicals may play a role in neuronal
cell death in retinal ischemia–reperfusion
This PDF is available to Subscribers Only