Purchase this article with an account.
J. Lee, S.E. Lee, Y.H. Yoon; Zinc Accumulation in Degenerating Retinal Neurons Following Pressure-induced Ischemia . Invest. Ophthalmol. Vis. Sci. 2003;44(13):466.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: Cytotoxicity mediated by endogenous zinc contributes to cell death in acute brain injury. Since the retina also contains releasable zinc, zinc-based cytotoxic mechanisms may contribute to retinal cell death in the setting of acute retinal injury. In the present study, we sought to determine the characteristics and the mechanism of zinc-induced cytotoxicity in the ischemic retinal neuronal death using an animal model. Methods: SD rats were used for experiments. The intraocular pressure was raised over systolic pressure to completely halt retinal arterial circulation by elevating the saline reservoir that was connected into the anterior chamber. Within 1 hour following 65 minutes of ischemia, either sodium pyruvate solution or normal saline was administered via the tail vein throughout the following 24 hours. Eyeballs were stained with TFL zinc-specific fluorescent staining and observed under the microscope.Results: Following 24 hours after the ischemia, Zinc accumulation was markedly increased in perikarya of the retinal cells especially in the inner neclear later. When treated with sodium pyruvate infusion, the degree of Zinc accumulation was significantly attenuated.Conclusions: Considering the evidence that zinc-based cytotoxicity plays an important role in various models of acute CNS injury, the cellular mechanism of zinc toxicity may be invloved in the retinal ischemic neuronal injury. The present results suggest that pyruvate may be effective in ameliorating zinc-triggered cell death in ischemic retina.
This PDF is available to Subscribers Only