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S.-W. Jung, I. Kim, M. Park, J.-I. Moon; Alteration of Superoxide Dismutase, Heme Oxygenase and Neuronal Nitric Oxide Synthetase Gene Expression After Glutathione Depletion in the Mouse Retina. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5546.
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Oxidative stress has been implicated in neuronal vulnerability. Different from other brain regions, retina is destined to be exposed to the light, resulting in higher levels of oxidative stress. In the absence of the defense mechanisms such as enzymatic anti-oxidant, the photosensitive oxidative stress may lead to extensive damage in the retina. Glutathione (GSH) is known to play a critical role in the cellular defense against unregulated oxidative stress in mammalian cells including neurons, and we previously demonstrated that GSH depletion induces cell death in the retina. Thus, we here examined expression of enzymatic anti-oxidant, heme oxygenase-1 (HO-1), superoxide dismutase1 and 2 (SOD1 and SOD2), and neuronal nitric oxide synthetase (nNOS) in both normal and oxidative stressed retina.
We induced the unregulated oxidative stress in the retina by depletion of intracellular GSH using buthionine sulphoximine (BSO), an inhibitor of γ-glutamylcysteine synthetase to mice. After 0, 1, 4, and 7 days of BSO administration, total RNAs from each animals were isolated and subjected to real-time RT-RCR analysis.
One day after BSO injection, expressions of ho-1 and n-nos were significantly increased, whereas expressions of sod were not changed. Expressions of ho-1 and n-nos decreased from 4 days after BSO injection. The expression of ho-1 was still higher than the basal level, whereas expression of n-nos was below the basal level. Expression of sod2 decreased from 4 days after BSO administration, whereas expression of sod1 was not altered.
We demonstrated that unregulated oxidative stress caused by glutathione depletion altered expressions of enzymatic anti-oxidant, sod2 and ho-1 and n-nos in distinct manners, suggesting that these enzymes may play different roles in the cellular defense against the unregulated oxidative stress in the retina. Alteration of HO-1, nNOS and SOD2 gene expression may provide a therapeutic tool for retinal degenerative diseases caused by the intracellular oxidative stress such as glaucoma.
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