Glaucoma Research Today is a free monthly online journal that collates and summarizes the latest research about Glaucoma, including details on cataracts, surgery, treatment, blindness. | ||||||||
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Oxidative stress is an early event in hydrostatic pressure induced retinal ganglion cell damage.Liu Q, Ju WK, Crowston JG, Xie F, Perry G, Smith MA, Lindsey JD, Weinreb RN Hamilton Glaucoma Center and the Department of Ophthalmology, University of California San Diego, La Jolla, California 92037-0946, USA. PURPOSE: To determine whether oxidative adduct formation or heme oxygenase-1 (HO-1) expression are altered in retinal ganglion cell (RGC) cultures exposed to elevated hydrostatic pressure and in a mouse model of glaucoma. METHODS: Cultured RGC-5 cells were subjected to 0, 30, 60, or 100 mm Hg hydrostatic pressure for 2 hours, and the cells were harvested. Parallel experiments examined the recovery from this stress, the effect of direct 4-hydroxy-2-nonenal (HNE) treatment, and the effect of pretreatment with resveratrol or quercetin. Mice were anesthetized and intraocular pressure was increased to 30, 60, or 100 mm Hg for 1 hour; then the retinas were harvested. HNE adduct formation and HO-1 expression were assessed by immunocytochemistry and immunoblotting. RESULTS: Increases of HNE-protein adducts (up to 5-fold) and HO-1 expression (up to 2.5 fold) in pressure-treated RGC-5 cells were dose dependent. During recovery experiments, HNE-protein adducts continued to increase for up to 10 hours; in contrast, HO-1 expression decreased immediately. HNE, at a concentration as low as 5 muM, led to neurotoxicity in RGC-5 cells. HNE adducts and HO-1 expression increased in the mouse retina and optic nerve after acute IOP elevation up to 5.5-fold and 2-fold, respectively. Antioxidant treatment reduced the oxidative stress level in pressure-treated RGC-5 cells. CONCLUSIONS: This study demonstrates that oxidative stress is an early event in hydrostatic pressure/IOP-induced neuronal damage. These findings support the view that oxidative damage contributes early to glaucomatous optic neuropathy. Published 27 September 2007 in Invest Ophthalmol Vis Sci, 48(10): 4580-9.
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