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.
Rabbit eyes, in vivo and in vitro, were exposed to UV-B irradiation at 300 nm, from a mercury arc lamp with an 11 nm bandpass filter. Radiant exposure ranged from 0.1 J/cm2 to 0.5 J/cm2. In vivo, swelling of the cornea resulted over a 12 to 40 hr period, the extent and duration being directly related to exposure. Recovery of normal thickness was complete within four days. Corneas removed at 18 hr after exposure recovered normal thickness during a five hour perfusion period, except for those most heavily exposed. When removed at 42 hr post exposure all corneas thinned to almost normal thickness. SEM showed the endothelial cells of exposed eyes to have either exaggerated villi on the surface and a disorganized mosaic or, after higher exposures, to be devoid of villi and have loose, flap like cell borders and large "blebs." After exposure of isolated corneas mounted for perfusion, swelling again ensued and similar changes were observed in the appearance of the cells, except that "blebs" were not found. No significant changes were observed in the metabolic components ATP, ascorbate and glutathione, nor was there any indication of lipid peroxidation. At higher in vivo exposures, the aqueous humor did show a decrease in ascorbate concentration and an increase in protein content, which probably result from a breakdown of the blood-aqueous barrier. UV-B irradiation may cause or promote changes in the endothelium associated with aging, but the one time radiant exposures of the magnitude used in this study, appear to have no severe or permanently toxic effects.
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