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Glutathione (GSH) and Eye Health:
Cataracts and Macular Degeneration

Glutathione: a vital lens antioxidant.
Giblin FJ. [J Ocul Pharmacol Ther. 2000 Apr;16(2):121-35.] The reducing compound glutathione (GSH) exists in an unusually high concentration in the lens where it functions as an essential antioxidant vital for maintenance of the tissue's transparency. In conjunction with an active glutathione redox cycle located in the lens epithelium and superficial cortex, GSH detoxifies potentially damaging oxidants such as H2O2 and dehydroascorbic acid. Recent studies have indicated an important hydroxyl radical-scavenging function for GSH in lens epithelial cells, independent of the cells' ability to detoxify H2O2. Depletion of GSH or inhibition of the redox cycle allows low levels of oxidant to damage lens epithelial targets such as Na/K-ATPase, certain cytoskeletal proteins and proteins associated with normal membrane permeability. The level of GSH in the nucleus of the lens is relatively low, particularly in the aging lens, and exactly how the compound travels from the epithelium to the central region of the organ is not known. Recently, a cortical/nuclear barrier to GSH migration in older human lenses was demonstrated by Sweeney et al. The relatively low ratio of GSH to protein -SH in the nucleus of the lens, combined with low activity of the glutathione redox cycle in this region, makes the nucleus especially vulnerable to oxidative stress, as has been demonstrated with use of in vivo experimental animal models such as hyperbaric oxygen, UVA light and the glutathione peroxidase knockout mouse. Effects observed in these models, which are currently being utilized to investigate the mechanism of formation of human senile nuclear cataract, include an increase in lens nuclear disulfide, damage to nuclear membranes and an increase in nuclear light scattering. A need exists for development of therapeutic agents to slow age-related loss of antioxidant activity in the nucleus of the human lens to delay the onset of cataract.

Protection of retinal pigment epithelium from oxidative injury by glutathione and precursors.
Sternberg P Jr, Davidson PC, Jones DP, Hagen TM, Reed RL, Drews-Botsch C. [Invest Ophthalmol Vis Sci. 1993 Dec;34(13):3661-8.]
This study was performed to examine the effect of exogenous glutathione (GSH) or its precursor amino acids on oxidative injury in cultured human retinal pigment epithelium (RPE). Added GSH provided protection at concentrations of 0.01 mM and higher. The amino acid precursors for GSH, glutamate, cysteine, and glycine also protected against injury, but this required at least 0.1 mM of each amino acid. These results indicate that protection by the amino acid precursors is mediated through synthesis of GSH, and they also show that exogenous GSH can provide protection against oxidative injury.

Glutathione in human plasma: Decline in association with aging, age- related macular degeneration, and diabetes
Samiec PS, Drews-Botsch C, and others. [Free Radic Biol Med 1998 Mar 15;24(5):699-704.] Blood samples were analyzed for GSH and GSH redox state in 40 age-related macular degeneration (ARMD) patients (> 60 y), 33 non-ARMD diabetic patients (> 60 years), 27 similarly aged non-ARMD and nondiabetic individuals (> 60 years), and 19 younger individuals (< 60 years) without ARMD or diabetes. Results showed a significantly lower plasma GSH in older individuals (ARMD, diabetes, and controls) than in younger individuals. The results suggest that in studies of age-related pathologies, oxidation of GSH may be a more important parameter than a decline in pool size, while in specific pathologies such as diabetes, both oxidation and a decline in pool size may be important.
Publication Types:
Clinical Trial
Controlled Clinical Trial

Glutathione peroxidase-1 deficiency leads to increased nuclear light scattering, membrane damage, and cataract formation in gene-knockout mice.
Reddy VN, Giblin FJ, Lin LR, Dang L, Unakar NJ, Musch DC, Boyle DL, Takemoto LJ, Ho YS, Knoernschild T, Juenemann A, Lutjen-Drecoll E. [Invest Ophthalmol Vis Sci. 2001 Dec;42(13):3247-55.] Previous in vitro studies with transgenic and gene-knockout mice have shown that lenses with elevated levels of glutathione peroxidase (GPX)-1 activity are able to resist the cytotoxic effect of H(2)O(2), compared with normal lenses and lenses from GPX-1-deficient animals. The purpose of this study was to investigate the functional role of this enzyme in antioxidant mechanisms of lens in vivo by comparing lens changes of gene-knockout mice with age-matched control animals. The results demonstrate the critical role of GPX-1 in antioxidant defense mechanisms of the lens nucleus.

Specialized protective role of mucosal glutathione in pigmented rabbit conjunctiva.
Gukasyan HJ, Kim KJ, Kannan R, Farley RA, Lee VH. [Invest Ophthalmol Vis Sci. 2003 Oct;44(10):4427-38.] To investigate mechanisms of H(2)O(2)-induced reduction in rates of active ion transport (I(sc)) across the pigmented rabbit conjunctival tissue and the protective role afforded by mucosal glutathione (GSH). ...actively secreted GSH by conjunctival epithelial cells may help reduce the injury by mucosally applied H(2)O(2). Injury by H(2)O(2) may directly affect vital membrane components (e.g., Na(+),K(+)-ATPase) involved in active ion transport across conjunctiva. Mucosal protection by GSH (or its analogues) of active conjunctival ion transport may be useful in maintaining the physiological functions of conjunctiva under oxidative stress.



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