No abstract

Oxygen levels in the eye are generally low and tightly regulated. Oxygen enters the eye largely by diffusion from retinal arterioles and through the cornea. In intact eyes, oxygen from the retinal arterioles diffuses into the vitreous body. There is a decreasing oxygen gradient from the retina to the lens, established by oxygen consumption by ascorbate in the vitreous fluid and lens metabolism. Age-related degeneration of the vitreous body or removal during vitrectomy exposes the posterior of the lens to increased oxygen, causing nuclear sclerotic cataracts. Lowering oxygen in the vitreous, as occurs in patients with ischemic diabetic retinopathy, protects against cataracts after vitrectomy. Vitrectomy and cataract surgery increase oxygen levels at the trabecular meshwork and with it the risk of open angle glaucoma. Two additional risk factors for glaucoma, African heritage and having a thinner cornea, are also associated with increased oxygen in the anterior chamber angle. Preservation of the vitreous body and the lens, two important oxygen consumers, would protect against nuclear sclerotic cataracts and open angle glaucoma. Delaying removal of the lens for as long as possible after vitrectomy would be an important step in delaying ocular hypertension and glaucoma progression.

The lens is composed of a thin metabolically active outer layer, consisting of epithelial and superficial fibre cells. Lying within this outer shell are terminally differentiated, metabolically inactive fibre cells, which are divided into an outer cortex and central nucleus. Mature fibre cells contain a very high protein concentration, which is important for the transparency and refractive power of the lens. These proteins are protected from oxidation by reducing substances, like glutathione, and by the low-oxygen environment around the lens. Glutathione reaches the mature fibre cells by diffusing from the metabolically active cells at the lens surface. With age, the cytoplasm of the nucleus becomes stiffer, reducing the rate of diffusion and making nuclear proteins more susceptible to oxidation. Low pO 2 is maintained at the posterior surface of the lens by the physical and physiological properties of the vitreous body, the gel filling the space between the lens and the retina. Destruction or degeneration of the vitreous body increases exposure of the lens to oxygen from the retina. Oxygen reaches the lens nucleus, increasing protein oxidation and aggregation and leading to nuclear cataract. We suggest that maintaining low pO 2 around the lens should prevent the formation of nuclear cataracts.

The prevalence of cortical cataract was higher in the lower nasal quadrant than in the other quadrants for all subjects of diverse race in three climatically different locations. This higher prevalence was most pronounced in subjects living at low latitude. These results support the view that solar UV exposure is a possible risk factor for development of human cortical cataract.

The purpose of this study was to investigate correlations of partial pressure of oxygen (pO 2 ) in the ocular anterior segment of human eyes and aqueous humor antioxidant levels of ascorbate (AsA) and total reactive antioxidant potential (TRAP) with glaucoma and vitreous status.METHODS: This prospective, cross-sectional study stratified patients (n [ 288 eyes) by lens and vitreous status and the presence of primary open-angle glaucoma for statistical analyses. Intraocular pO 2 concentrations were measured using a fiberoptic probe in patients at the beginning of planned glaucoma and/or cataract surgery. Aqueous humor specimens were obtained for antioxidant analysis of AsA and TRAP.RESULTS: Following prior pars plana vitrectomy, pO 2 levels were significantly higher than in the reference group of cataract surgery in the anterior chamber angle (16.2 ± 5.0 vs. 13.0 ± 3.9 mm Hg; P [ .0171) and in the posterior chamber (7.6 ± 3.1 vs. 3.9 ± 2.7 mm Hg; P < .0001). AsA and TRAP levels were significantly lower (1.1 ± 0.4 vs. 1.4 ± 0.5 mM, respectively; 403.3 ±116.5 vs. 479.0 ± 146.7 Trolox units, respectively; P [ .004 and P [ .024, respectively) in patients after vitrectomy. In patients with an intact vitreous, neither pO 2 nor antioxidant status correlated with lens status or glaucoma.CONCLUSIONS: Increased pO 2 and antioxidant depletion following vitrectomy suggests an alteration of the intraocular oxidant-antioxidant balance. Our study links physiologic factors such as increased pO 2 in the anterior chamber angle and the posterior chamber to decreased antioxidant levels in aqueous humor following vitrectomy. Oxidative stress/ damage to the trabecular meshwork in such postvitrectomy cases may contribute to intraocular pressure elevation and increased risk of glaucoma. NOTE: Publication of this article is sponsored by the American Ophthalmological Society.

No abstract

The authors have conducted cataract epidemiological studies in four climatically and racially different places and compared the data. The survey places were Noto and Amami in Japan, Reykjavik in Iceland, and Singapore. The evaluation and grading of lens opacities were done using graphic analysis of Scheimpflug and retro-illumination images. The prevalence of nuclear opacity was extremely high in the Singapore group, followed by Amami. The main type of lens opacity was nuclear in the Singapore group and cortical in the Noto and Icelandic groups. The characteristic lens opacity in Amami was in between the above two groups. No significant difference was seen in the prevalence of nuclear opacity between males and females in any of the groups. Although the common factors of the living conditions in the subjects with a high prevalence of nuclear opacity appear to be high UV exposure and high ambient temperature, future investigations should be made to disclose the possible cause.

Purpose To quantify the relationship between 1H longitudinal relaxation rate constant, R1, and O2 concentration (relaxivity, r1) in tissue and to quantify O2-driven changes in R1 (ΔR1) during a breathing gas challenge in normal brain, radiation-induced lesions, and tumor lesions. Methods Relaxivity determination. R1 data were collected in control-state mice (n=4) during three different breathing gas (and thus tissue O2) conditions. In parallel experiments, pO2 was measured in the thalamus of control-state mice (n=4) under the same breathing gas conditions using an O2-sensitive micro-probe. The relaxivity of tissue O2 was calculated using the R1 and pO2 data. Pathology determination. R1 data were collected in control-state (n=4) mice, a glioma model (n=7), and a radiation necrosis model (n=6) during two breathing gas (thus tissue O2) conditions. R1 and ΔR1 were calculated for each cohort. Results O2 r1 in the brain was 9×10−4±3×10−4 mmHg−1s−1 at 4.7T. R1 and ΔR1 measurements distinguished radiation necrosis from tumor (p<0.03 and p<0.01, respectively). Conclusion The relaxivity of O2 in brain is determined. R1 and ΔR1 measurements differentiate tumor lesions from radiation necrosis lesions in the mouse models. These pathologies are difficult to distinguish by traditional imaging techniques; O2-driven changes in R1 holds promise in this regard.