Glutathione Peroxidase in Lens and a Source of Hydrogen Peroxide in Aqueous Humour

Pirie, Antoinette

doi:10.1042/bj0960244

Cited by 161 publications

(31 citation statements)

References 19 publications

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“…This finding is consistent with a previous study [27]. GSH-Px in the lens was first shown by Pirie [28]. Significant decreased activity of GSH-Px in cataractous lenses was reported previously [9,10,29].…”

Section: Discussionsupporting

confidence: 83%

Superoxide Dismutase, Catalase, Glutathione Peroxidase and Xanthine Oxidase in Diabetic Rat Lenses

et al. 1999

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The activities of the protective enzymes, superoxide dismutase, catalase, glutathione peroxidase and of xanthine oxidase, an enzyme acting as a source of O^–₂, were measured in the lenses of alloxan-induced diabetic and control rats. Superoxide dismutase and glutathione peroxidase activities were found to be significantly decreased, while catalase and xanthine oxidase activities were increased. This means that the ratio of the oxidant/antioxidant enzymes increases in the diabetic rat lens, suggesting an increased oxidative stress. This imbalance is possibly an important contributing factor in the pathogenesis of diabetic cataract.

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Section: Discussionsupporting

confidence: 83%

Superoxide Dismutase, Catalase, Glutathione Peroxidase and Xanthine Oxidase in Diabetic Rat Lenses

et al. 1999

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“…Ascorbate and H2O; were analyzed by the DCPIP method of Pirie [25], since both solutes could be quantified in the same aliquot of aqueous humor. Samples were run at 610 nm in a Beckman DU7 spec trophotometer with a slight modification of the meth odology to allow accurate quantitation of H2O2 con centrations.…”

Section: Methodsmentioning

confidence: 99%

Roles of Catalase and the Glutathione Redox Cycle in the Regulation of Anterior-Chamber Hydrogen Peroxide

1991

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The effects of inhibition of both glutathione synthesis and of glutathione reductase and catalase activities have been determined in the regulation of hydrogen peroxide (H₂O₂) in the anterior chamber of pigmented rabbits. Glutathione reductase inhibition using intravitreal 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) did not significantly alter either total glutathione or the percent oxidized glutathione fraction in the iris-ciliary body. Intravitreal buthionine sulfoximine (BSO) significantly reduced the total glutathione content of iris-ciliary body and corneal endothelium, while not altering the oxidized fraction. BCNU increased the oxidized fraction of glutathione in the aqueous humor from 22 to 63% without significantly altering total glutathione levels. BSO, however, reduced total glutathione by 70% in the aqueous humor, and the oxidized fraction doubled. Decreases in the reduced glutathione concentration caused by BSO correlate with increases in the normally stable ratio of H₂O₂ to ascorbate concentrations in the aqueous humor, strongly suggesting that glutathione metabolism is correlated with H₂O₂ regulation at endogenous levels of this oxidant. Both BSO and 3-aminotriazole (3AT) separately increased the half-time for the loss of exogenously added H₂0₂ from the anterior chamber. BSO increased the half-time by 77% after 10 μl of 10 mMH₂O₂ was injected intracamerally, while suppression of catalase activity with 3AT increased it by only 40%. With intracameral injections of 10 μl of either 25 or 50 mM H₂O₂, however, 3AT had a greater effect than BSO. The half-time values after 3AT pretreat-ment were 61 and 135% greater than control values at the concentrations of 25 and 50 mM H₂O₂, respectively; those after BSO pretreatment were at 14 and 78%. From these data we conclude that the glutathione redox system protects the anterior segment tissues from hydrogen peroxide at low concentrations of this oxidant, while catalase assumes a greater role at higher concentrations of hydrogen peroxide.

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“…GSH was determined by the method of Ellman (1959). Ascorbic acid was determined by titration with 2,6-dichlorophenol-indophenol (Pirie, 1965). Protein was determined as described by Robinson & Hogden (1940).…”

Section: Methodsmentioning

confidence: 99%

The metabolism of naphthalene and its toxic effect on the eye

Pirie

1967

Biochemical Journal

127

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1. Naphthalene (1g./kg.) was fed daily by stomach tube to rabbits. 2. In more than half of the rabbits opacities in the lens and degeneration of the retina were visible in vivo. 3. Dissection of eye tissues revealed some or all of the following changes: a browning of the lens and eye humours, blue fluorescence of the eye humours and crystals in the retina and vitreous body. 4. The ascorbic acid concentration of the eye humours was decreased. 5. Some metabolites of naphthalene [1,2-dihydro-1,2-dihydroxynaphthalene, 2-hydroxy-1-naphthyl sulphate and (1,2-dihydro-2-hydroxy-1-naphthyl glucosid)uronic acid] are converted enzymically by the tissues of the eye into 1,2-dihydroxynaphthalene. 6. Changes in the eye are consistent with 1,2-dihydroxynaphthalene's being the primary toxic agent. The properties and reactions of this substance are described. 7. 1,2-Dihydroxynaphthalene is readily autoxidizable in neutral solution to form the yellow 1,2-naphthaquinone and hydrogen peroxide. This oxidation is reversed by ascorbate. 8. Ascorbate is oxidized catalytically by 1,2-naphthaquinone. This may account for the disappearance of ascorbate from the aqueous and vitreous humours of the eye after naphthalene feeding. It may also account for the appearance of crystals of calcium oxalate in the eye. 9. The brown colour of the lens of the naphthalene-fed rabbit is due to presence of naphthaquinone-protein compounds.

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Glutathione Peroxidase in Lens and a Source of Hydrogen Peroxide in Aqueous Humour

Cited by 161 publications

References 19 publications

Superoxide Dismutase, Catalase, Glutathione Peroxidase and Xanthine Oxidase in Diabetic Rat Lenses

Superoxide Dismutase, Catalase, Glutathione Peroxidase and Xanthine Oxidase in Diabetic Rat Lenses

Roles of Catalase and the Glutathione Redox Cycle in the Regulation of Anterior-Chamber Hydrogen Peroxide

The metabolism of naphthalene and its toxic effect on the eye

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