Automatic estimation of the cross-sectional area of the waist of the nerve fibre layer at the optic nerve head.

PURPOSE: Glaucoma leads to pathological loss of axons in the retinal nerve fibre layer at the optic nerve head (ONH). This study aimed to develop a strategy for the estimation of the cross-sectional area of the axons in the ONH. Furthermore, improving the estimation of the thickness of the nerve fibre layer, as compared to a method previously published by us. METHODS: In the 3D-OCT image of the ONH, the central limit of the pigment epithelium and the inner limit of the retina, respectively, were identified with deep learning algorithms. The minimal distance was estimated at equidistant angles around the circumference of the ONH. The cross-sectional area was estimated by the computational algorithm. The computational algorithm was applied on 16 non-glaucomatous subjects. RESULTS: The mean cross-sectional area of the waist of the nerve fibre layer in the ONH was 1.97 ± 0.19 mm2 . The mean difference in minimal thickness of the waist of the nerve fibre layer between our previous and the current strategies was estimated as CIµ (0.95) 0 ± 1 µm (d.f. = 15). CONCLUSIONS: The developed algorithm demonstrated an undulating cross-sectional area of the nerve fibre layer at the ONH. Compared to studies using radial scans, our algorithm resulted in slightly higher values for cross-sectional area, taking the undulations of the nerve fibre layer at the ONH into account. The new algorithm for estimation of the thickness of the waist of the nerve fibre layer in the ONH yielded estimates of the same order as our previous algorithm.

Dose-response relationship for α-tocopherol prevention of ultraviolet radiation induced cataract in rat.

The purpose of this study is to establish the dose response relationship for α-tocopherol protection of ultraviolet radiation (UVR) induced cataract in the rat. Four groups of 20 six-week-old albino Sprague Dawley rats received 5, 25, 50, and 100 IU/day α-tocopherol, whilst another group of 20 rats without any α-tocopherol feeding was the control group. After 4 weeks of feeding, each rat was unilaterally exposed to 8 kJ/m(2) UVR-300 nm for 15 min. At 1 week after exposure, the rats were sacrificed and lens light scattering was measured quantitatively. Lens total reduced (GSH) and oxidized (GSSG) glutathione; glutathione reductase (GR) and peroxidase (GPx) were determined spectrophotometrically. The UVR-exposed lenses in the α-tocopherol fed groups developed superficial cataract, whereas lenses in the control group developed cortical and equatorial opacities. Light scattering in lenses from the α-tocopherol-supplemented rats was lower than in lenses from the control group. The difference of light scattering between the exposed and contralateral non-exposed lens decreased with increasing doses of α-tocopherol to an asymptote level. UVR-exposure caused a significant depletion of lens GSH in rats without or at low α-tocopherol supplementation. The depletion of GSH became less with higher α-tocopherol supplementation. There was no detectable difference in lens GSSG, GR or GPx at any level of α-tocopherol supplementation. Orally administered α-tocopherol dose dependently protects against UVR-induced cataract. The protection is associated with an α-tocopherol dose-dependent GSH depletion secondary to UVR exposure. UVR-induced light scattering only occurs if the GSH depletion exceeds a threshold.

Variance components for PIMD-2π estimation of the optic nerve head and consequences in clinical measurements of glaucoma.

PURPOSE: To estimate the sources of variation for Pigment epithelium central limit-Inner limit of the retina Minimal Distance averaged over 2π (PIMD-2π), and further to analyse their consequences for clinical measurements of glaucoma. METHODS: Forty subjects with early to moderate stage glaucoma were included. Three SD-OCT volumes of the optic nerve head (ONH) were captured at two occasions. Each volume was segmented three times for PIMD-2π. The magnitude of the sources of variation for PIMD-2π measurements was estimated with an analysis of variance. RESULTS: A 95% confidence interval for mean PIMD-2π was estimated to 215 ± 12 µm (df = 38). The estimated variance for subjects was 1280 µm2 . The within-subject estimated variance for occasions, volumes and segmentations was 10 µm2 , 30 µm2 and 40 µm2 , respectively. The within-subject variances were used to model follow-up of PIMD-2π over time. A linear loss rate of 0.05 of baseline PIMD-2π/year was assumed. A significant PIMD-2π change could be detected in approximately 16-18 months with evenly spaced visits every 4 or 6 months. CONCLUSIONS: Due to the small within-subject estimated variances, a clinically undesirable PIMD-2π change from baseline can be detected in approximately 18 months. Detection of significant PIMD-2π loss in a subject requires knowledge of normal age loss and measurement variability.

A strategy for OCT estimation of the optic nerve head pigment epithelium central limit-inner limit of the retina minimal distance, PIMD-2π.

PURPOSE: To develop a semi-automatic algorithm for estimation of pigment epithelium central limit-inner limit of the retina minimal distance averaged over 2π radians (PIMD-2π) and to estimate the precision of the algorithm. Further, the variances in estimates of PIMD-2π were to be estimated in a pilot sample of glaucomatous eyes. METHODS: Three-dimensional cubes of the optic nerve head (ONH) were captured with a commercial SD-OCT device. Raw cube data were exported for semi-automatic segmentation. The inner limit of the retina was automatically detected. Custom software aided the delineation of the ONH pigment epithelium central limit resolved in 500 evenly distributed radii. Sources of variation in PIMD estimates were analysed with an analysis of variance. RESULTS: The estimated variance for segmentations and angles was 130 µm2 and 1280 µm2 , respectively. Considering averaging eight segmentations, a 95 % confidence interval for mean PIMD-2π was estimated to 212 ± 10 µm (df = 7). The coefficient of variation for segmentation was estimated at 0.05. In the glaucomatous eyes, the within-subject variance for captured volumes and for segmentations within volumes was 10 µm2 and 50 µm2 , respectively. CONCLUSION: The developed semi-automatic algorithm enables estimation of PIMD-2π in glaucomatous eyes with relevant precision using few segmentations of each captured volume.

p53 expression and apoptosis in the lens after ultraviolet radiation exposure.

PURPOSE: To localize p53 protein and active caspase-3 in the albino rat lens and to compare p53 mRNA and active caspase-3 expression in ultraviolet radiation (UVR) 300 nm exposed lenses and their contralateral nonexposed controls. METHODS: Ten Sprague-Dawley albino rats were unilaterally exposed to 8 kJ/m(2) UVR, and the contralateral eyes were left nonexposed. In total, four exposed lenses and their respective contralateral nonexposed lenses were analyzed by immunohistochemistry to localize p53 and active caspase-3. In addition, six exposed and contralateral nonexposed lenses were analyzed by real-time RT-PCR. Quantified p53 and caspase-3 expression were compared between the in vivo UVR 300 nm exposed lenses and the contralateral nonexposed lenses. RESULTS: All lenses exposed to UVR developed cataract. Immunohistochemistry showed that p53 and active caspase-3 were localized in the lens epithelial cells. Quantified p53 and caspase-3 expression were significantly higher in lenses exposed to UVR than in nonexposed lenses. CONCLUSIONS: p53 and caspase-3 expression increase in lens epithelial cells after UVR exposure. In the lens, apoptosis induced by UVR may be associated with increased p53 expression.

Biological response in various compartments of the rat lens after in vivo exposure to UVR-B analyzed by HR-MAS 1H NMR spectroscopy.

PURPOSE: The purpose of the present study was to investigate metabolic changes in different compartments of the rat lens (anterior, nuclear, posterior, and equatorial) after exposure to an acute double threshold dose of ultraviolet-B radiation (UVR-B) by using high-resolution magic angle spinning (HR-MAS) (1)H nuclear magnetic resonance (NMR) spectroscopy and pattern recognition (PR) METHODS: methods. One eye in each of 28 6-week-old female albino Sprague-Dawley rats was exposed to in vivo 7.5 kJ/m2 UVR-B for 15 minutes. The contralateral eye was left unexposed. One week after irradiation, all rats were killed, and both lenses were isolated. Each lens was cored by a trephine, and the cylinder was sliced into three portions (anterior, nuclear, and posterior). The lens material that remained after the coring process was analyzed as the equatorial region. Analysis of lens metabolism was performed by HR-MAS 1H NMR spectroscopy (14.1 T; Avance DRX600; Bruker BioSpin GmbH, Rheinstetten, Germany), and the metabolic profiles were statistically analyzed by the PR method of principal component analysis (PCA). RESULTS: Metabolic differences were detected among the compartments in the lens, both in samples from the contralateral nonexposed lenses and in samples from lenses exposed to in vivo UVR-B. In the rat lens, exposure to UVR-B caused changes in GSH, phosphocholine, myo-inositol, succinate, formate, and adenosine triphosphate (ATP)/adenosine diphosphate (ADP) and in levels of the amino acids phenylalanine, taurine, hypo-taurine, tyrosine, alanine, valine, isoleucine, and glutamate, that varied among lens compartments. CONCLUSIONS: HR-MAS 1H NMR spectroscopy, combined with PR methods (PCA), is effective for analysis of separate parts of the intact rat lens. To understand the biochemistry of the lens, it is important to divide the lens into sections, representing functionally and anatomically distinct compartments.

Variance components in confocal scanning laser tomography measurements of neuro-retinal rim area and the effect of repeated measurements on the power to detect loss over time.

PURPOSE: To estimate the variation in measurements of neuro-retinal rim area (NRA) determined by confocal scanning laser tomography and consequences for clinical follow-up. METHODS: Altogether, 24 healthy subjects were randomized on -320 µm, Moorfields and Standard NRA plane strategies. Additionally, NRA was measured in 32 glaucoma subjects. Variance components for subjects, visits and measurements were estimated with analysis of variance. Sample sizes required to detect a 6.0 × 10-2  mm2 NRA change were estimated assuming a significance level of 0.05 and a power of 0.8. Consequences for independent group, and paired comparison design, respectively, were analysed. Further, precision in estimates within subjects over time was investigated. RESULTS: The variation of NRA among subjects was considerably larger than the variation among visits and measurements. For glaucoma subjects, the variation among visits and measurements were of the same order but larger than in healthy subjects. It was found that independent group comparisons require inconveniently large sample sizes. Within-subject paired comparisons over time require sample sizes of below 15 subjects. The estimated variations for glaucoma subjects imply that 54 months of follow-up is required for detection of change from baseline. CONCLUSIONS: The variance for subjects is substantial in relation to those for visits and measurements. Cross-sectional independent group comparisons of levels of NRA are unsuitable, due to considerable subject variation. Levels of NRA differences within subjects between visits can be estimated with acceptable precision. Neuro-retinal rim area (NRA) measurement can be used for long-term follow-up of glaucoma progression.

1090 nm infrared radiation at close to threshold dose induces cataract with a time delay.

PURPOSE: To investigate whether infrared radiation (IRR)-induced cataract is instant or is associated with a time delay between the exposure and the onset of lens light scattering after an exposure to just above threshold dose. METHODS: Six-weeks-old albino Sprague-Dawley female rats were unilaterally exposed to 197 W/cm2 IRR at 1090 nm within the dilated pupil. In the first experiment, the animals were exposed with four exposure times of 5, 8, 13 and 20 second, respectively. At 24 hr after exposure, the light scattering in both exposed and contralateral not exposed lenses was measured. Based on the first experiment, four postexposure time groups were exposed unilaterally to 1090 nm IRR of 197 W/cm2 for 8 second. At 6, 18, 55 and 168 hr after exposure, the light scattering in both lenses was measured. RESULTS: A 197 W/cm2 IRR-induced light scattering in the lens with exposures of at least 8 second. Further, after exposure to IRR of 197 W/cm2 for 8 second, the light-scattering increase in the lens was delayed approximately 16 hr after the exposure. CONCLUSION: There is a time delay between the exposure and the onset of cataract after exposure to close to threshold dose implicating that either near IRR cataract is photochemical or there is a time delay in the biological expression of thermally induced damage.

Lamellar changes in the keratoconic cornea.

PURPOSE: The purpose of this study was to identify ultrastructural changes associated with ectasia and to determine the association between lamellar count and corneal thinning. METHODS: Five surgically removed keratoconic corneal buttons and four, non-keratoconic, normal eye bank control corneas were processed for transmission electron microscopy using an established protocol, ensuring minimal tissue distortion. A sequence of overlapping digital images, spanning the full apical cone corneal thickness, was assembled. A seamless digital montage was printed at 5000× magnification. Lamellae were counted in the anterior-posterior orientation, along a linear line, using established criteria for identification of individual lamellae. RESULTS: The stromal thickness estimated as a 95% confidence interval for the mean, CI (0.95), in the keratoconic corneas was 372 ± 62 µm, while in the normal cornea, it was 446 ± 89 µm. All keratoconic corneas showed ultrastructural evidence of lamellar splitting and a loss of interweaving anterior lamellae. In the keratoconic corneas, the median total linear stromal lamellar absolute count tangential to the corneal surface was 362, (25th percentile; 75th percentile) = (355; 365) lamellae and in the normal cornea, 246, (25th percentile; 75th percentile) = (239; 251). The linear lamellar density in the keratoconic corneas was estimated as CI (0.95) 117 ± 22 and 86 ±19 lamellae per 100 µm in the anterior and posterior portion of the stroma, respectively. In normal cornea, the linear lamellar density was estimated as CI (0.95) 51 ± 8 and 80 ± 20 lamellae per 100 µm. The mean difference of linear lamellar count between the anterior and the posterior portion of the cornea was estimated as CI (0.95) 31 ± 23 for keratoconic corneas and -29 ± 28 for the normal corneas. CONCLUSIONS: The current morphometric analysis of ultrastructural changes suggests that ectasia and thinning in keratoconus is associated with lamellar splitting into multiple bundles of collagen fibrils and loss of anterior lamellae. These structural changes, possibly in addition to lateral shifting of lamellae due to the pressure gradient over the cornea, are a potential explanation to the central loss of mass.

Impact of age and sex in ultraviolet radiation cataract in the rat.

PURPOSE: The purpose of this study was to determine the influence of age and sex on the development of ultraviolet radiation (UVR) cataract in rats. Current safety limits for lens damage due to UVR do not consider age or sex. METHODS: Four age groups of Sprague-Dawley rats (3, 6, 17, and 52 weeks) were exposed to 300-nm UVR at either 5 or 8 kJ/m(2), delivered during 15 minutes. The interval between irradiation and cataract assessment was 1 or 8 weeks. Moreover, two groups of 6-week-old male and female rats were exposed to 5 kJ/m(2) UVR, with cataract assessment after 1 week. The severity of cataract was quantified by measurement of forward light-scattering in isolated lenses. RESULTS: The youngest age group showed development of anterior subcapsular, equatorial, and nuclear cataract, whereas the three older groups exhibited the first two types. The two younger age groups had significantly more cataract than the other groups. The degree of cataract increased from 1 to 8 weeks after irradiation. There was no difference in cataract severity between sexes. CONCLUSIONS: Young rats are more sensitive to UVR than old rats. Nuclear UVR cataract develops in young rats but not in adult rats. With the chosen waveband and dose, the time for maximum cataract development to occur is longer than 1 week. There is no difference in UVR sensitivity between the sexes.

Ultraviolet radiation-induced cataract: age and maximum acceptable dose.

PURPOSE: To investigate the effect of age on ultraviolet radiation-B (UVR-B)-induced cataract and to detect the maximum acceptable dose in rats of different age groups. METHODS: Four age groups of 20 rats each, aged 3, 6, 10, and 18 weeks, were included. Each age group was divided into five UVR-B dose subgroups. The rats were unilaterally exposed to UVR-B (lambda(max) = 302.6 nm, lambda(0.5) = 4.5 nm). The incident dose on the cornea varied between 0 and 8 kJ/m(2). One week after exposure, the rats were killed, both lenses were extracted, the intensity of forward light-scattering was measured, and photographs were taken. The sensitivity of the lens to UVR-B was estimated as the maximum acceptable dose. RESULTS: The maximum acceptable dose for 3-, 6-, 10-, and 18-week-old rats was estimated to be 1.4, 2.7, 4.3 and 5.2 kJ/m(2), respectively. CONCLUSIONS: Young rats were more sensitive to UVR-B than old ones. Age should be considered when estimating the risk for UVR-B-induced cataract.

Metabolic changes in rat lens after in vivo exposure to ultraviolet irradiation: measurements by high resolution MAS 1H NMR spectroscopy.

PURPOSE: In the present study, high-resolution magic angle spinning proton nuclear magnetic resonance (HR-MAS (1)H NMR) spectroscopy was used to investigate changes in the metabolic profile of intact rat lenses after UVB irradiation of the eyes. METHODS: Three groups of Sprague-Dawley rats were exposed to UVB radiation at 2.5, 5.0, and 7.5 kJ/m(2). One eye was exposed, and the contralateral eye served as the control. One week after exposure, the lenses were removed and forward light-scattering was quantified. Thereafter, proton NMR spectra from the intact lenses were obtained. Relative changes in metabolite concentrations were determined. RESULTS: The lenses in all three groups showed significant increases in light-scattering after UVB irradiation. The high-quality HR-MAS (1)H NMR spectra permitted more than 30 different metabolites to be identified. UVB irradiation caused a significant decrease (P < 0.05) in concentrations of taurine, hypotaurine, tyrosine, phenylalanine, valine, myo-inositol, phosphocholine, betaine, succinate, and glutathione at all three UV doses. For glycine, glutamate, and lactate, significant decreases in concentration were observed at the two lowest UVR-B doses. The total amount of adenosine tri- and diphosphate and (ATP, ADP) decreased significantly and that of adenosine monophosphate AMP increased significantly at the two highest doses. Alanine was the only amino acid that increased after UVB irradiation. None of these metabolites exhibited a significant UVB dose-dependent relationship. CONCLUSIONS: This study demonstrates for the first time the potential of HR-MAS (1)H NMR spectroscopy as an analytical tool for use on intact lenses. Near-threshold UVR-B doses led to a generally significant decrease in water-soluble metabolites 1 week after exposure. The lack of dose-dependent changes in the metabolites indicates that repair processes during the first week after UVB irradiation overcome the immediate metabolic disturbances.

Ocular temperature elevation induced by threshold in vivo exposure to 1090-nm infrared radiation and associated heat diffusion.

An in vivo exposure to 197 W/cm 2 1090-nm infrared radiation (IRR) requires a minimum 8 s for cataract induction. The present study aims to determine the ocular temperature evolution and the associated heat flow at the same exposure conditions. Two groups of 12 rats were unilaterally exposed within the dilated pupil with a close to collimated beam between lens and retina. Temperature was recorded with thermocouples. Within 5 min after exposure, the lens light scattering was measured. In one group, the temperature rise in the exposed eye, expressed as a confidence interval (0.95), was 11±3°C at the limbus, 16±6°C in the vitreous behind lens, and 16±7°C on the sclera next to the optic nerve, respectively. In the other group, the temperature rise in the exposed eye was 9±1°C at the limbus and 26±11°C on the sclera next to the optic nerve, respectively. The difference of forward light scattering between exposed and contralateral not exposed eye was 0.01±0.09 tEDC. An exposure to 197 W/cm 2 1090-nm IRR for 8 s induces a temperature increase of 10°C at the limbus and 26°C close to the retina. IRR cataract is probably of thermal origin.

Ultrastructure of UVR-B-induced cataract and repair visualized with electron microscopy.

PURPOSE: The aim of the study is to investigate and visualize the ultrastructure of cataract morphology and repair, after in vivo exposure to double threshold dose UVR-B in the C57BL/6 mouse lens. METHODS: Twenty-six-week-old C57BL/6 mice received in vivo double threshold dose (6.4 kJ/m2) UVR-B for 15 min. The radiation output of the UVR-source had λMAX at 302.6 nm. After a latency period of 1, 2, 4 and 8 days following UVR-B exposure, the induced cataract was visualized with electron microscopy techniques. Induced, cataract was quantified as forward lens light scattering. Damage to the lens epithelium and the anterior cortex was investigated with light microscopy in toluidine blue-stained semi-thin sections, transmission electron microscopy (TEM), scanning electron microscopy (SEM) and dark field illumination photography. RESULTS: UVR-B-exposed lenses developed anterior subcapsular and/or cortical and nuclear cataract after 1 day. Lens light scattering peaked 2 days after exposure. Lens epithelial cell damage was seen in TEM as apoptotic cells, apoptotic bodies, nuclear chromatin condensation, and swollen and disrupted anterior cortex fibres throughout the sections of the whole anterior lens surface. These morphologic changes were also visualized with SEM. Within 8 days, anterior subcapsular cataract was repaired towards the anterior sutures. CONCLUSION: UVR-B exposure of double cataract threshold dose induces a subtotal loss of epithelial cells across the whole anterior surface of the lens. This damage to the epithelium is repaired by epithelial cell movement from the equator towards the lens sutures, thus in retrograde direction to regular epithelial cell differentiation.

Evolution of TUNEL-labeling in the rat lens after in vivo exposure to just above threshold dose UVB.

PURPOSE/AIM: To quantitatively analyse the evolution of TUNEL-labeling, after in vivo exposure to UVB. METHODS: Altogether, 16 Sprague Dawley rats were unilaterally exposed in vivo for 15 min to close to threshold dose, 5 kJ/m(2), of ultraviolet radiation in the 300 nm wavelength region. Animals were sacrificed in groups of 4 at 1, 5, 24 and 120 h after exposure. For each animal, both eye globes were removed and frozen. The frozen eye was cryo-sectioned in 10 µm thick midsagittal sections. From each globe, three midsagittal sections with at least five sections interval in between were mounted on a microscope slide. Sections were TUNEL-labeled and counter stained with DAPI. For quantification of apoptosis, a fluorescence microscope was used. In sections with a continuous epithelial cell surface, the number of lens epithelial cell nuclei and the number of TUNEL-positive epithelial cell nuclei was counted. The total number of TUNEL-positive epithelial cell nuclei for all three sections of one lens in relation to the total number of epithelial cell nuclei for all three sections of the same lens was compared between exposed and contralateral not exposed lens for each animal. RESULTS: The relative difference of the fraction of TUNEL-positive nuclei between exposed and contralateral not exposed lens increased gradually, peaked in the time interval 5-120 h after exposure, and then declined. CONCLUSIONS: Close to threshold dose of UVB induces TUNEL-labeling that peaks in the time window 5-120 h after exposure to UVB.

The 7-year cumulative incidence of cornea guttata and morphological changes in the corneal endothelium in the Reykjavik Eye Study.

PURPOSE: To examine the corneal endothelium and establish the 7-year cumulative incidence of cornea guttata (CG). METHODS: Population-based prospective cohort study with 573 participants (third wave of the Reykjavik Eye Study (RES) in 2008). Four hundred and thirty-seven subjects had either right or left eyes available for analysis after excluding confounding eye conditions. The baseline for eyes at risk for developing CG is the second wave of the RES in 2001. Participants underwent specular microscopy and a standardized eye examination. RESULTS: The cumulative 7-year incidence of CG in either eye was estimated as a 95% confidence interval for the expected value for both genders combined (15-23%), for males (8-18%) and for females (19-29%). In right eye only, the 7-year cumulative incidence for both genders combined was estimated to be 6-11%. For genders combined and for males only, the data indicated no correlation between 7-year cumulated incidence and age at baseline. In women, however, the change of 7-year incidence for CG in at least one eye appeared to be correlated to age at baseline. Reduction of endothelial cell density for corneas with CG at baseline was found [CI (0.95)-132 ± 94]. CONCLUSION: The cumulative 7-year incidence of primary central CG for a middle-aged and older Caucasian population without history of potentially confounding eye disease has been established. Women tend to have higher incidence if onset occurs at middle age. If CG is present, the cell density and the cell size variation decrease within a 7-year period.

Impact of iris pigment and pupil size in ultraviolet radiation cataract in rat.

PURPOSE: To investigate the effect of iris pigment and pupil size in ultraviolet radiation (UVR)-induced cataract. METHODS: Brown-Norway rats (pigmented) and Fischer-344 rats (non-pigmented) were unilaterally exposed in vivo to 5 kJ/m(2) UVR. Each strain was split into two groups, each receiving either mydriatic (tropicamide) or miotic (pilocarpine) eye-drops. One week after exposure, the degree of ocular inflammation and damage in the anterior segment was determined. The lenses were extracted, photographed and the degree of forward light scattering (cataract) was quantified. RESULTS: The cataract types differed between the two strains. All Fischer rats developed macroscopically identifiable UVR cataract while only 41% of Brown-Norway rats did so. All groups except the miotic Brown-Norway developed significant light scattering. The Fischer rats developed 3-4-fold more lens light scattering than the Brown-Norway rats. The miotic Fischer group exhibited significantly more light scattering than the mydriatic Fischer group. There was no significant difference in light scattering between the two Brown-Norway groups. There was a correlation between ocular inflammation and degree of light scattering, with Brown-Norway rats exhibiting less inflammation and lens light scattering. CONCLUSIONS: Pigmented rats develop less UVR cataract and less ocular inflammation than non-pigmented rats. Pupil size plays a smaller role in UVR cataract development in pigmented rats than in non-pigmented. The role of UVR-induced ocular inflammation in cataract development is still ambiguous.

High lenticular tolerance to ultraviolet radiation-B by pigmented guinea-pig; application of a safety limit strategy for UVR-induced cataract.

PURPOSE: The purpose of this study was to determine a threshold measure, maximum tolerable dose (MTD), for avoidance of UVR-B-induced cataract in the pigmented guinea-pig. METHODS: Thirty pupil-dilated anesthetized young female guinea-pigs, divided into five equal groups, received between 0 and 84.9 kJ/m(2) unilateral UVR-B. Lens extraction and in vitro lens photography occurred 24 hr after exposure. Measurement of intensity of lens light scattering served as quantifying tool for the degree of cataract. Data analysis included regression, using a second order polynomial model. The applied MTD concept was based on the UVR-B dose-response curve obtained for the pigmented guinea-pig. A smaller number of pigmented guinea-pigs, pigmented rats and albino rats underwent morphometric analysis of the anterior segment geometry. RESULTS: All eyes exposed to UVR-B developed cataract in the anterior subcapsular region. MTD for avoidance of UVR-B-induced cataract was 69.0 kJ/m(2) in the pigmented guinea-pig. Iris was considerably thicker in the guinea-pig than in the rats. Lens blockage by the dilated iris was lowest in the guinea-pig. CONCLUSIONS: Maximum tolerable dose for avoidance of UVR-B-induced cataract in the pigmented guinea-pig was 69.0 kJ/m(2), over 10-fold higher than the threshold 5 kJ/m(2) obtained by Pitts et al. in the pigmented rabbit. Maximum tolerable dose is an appropriate method for estimation of toxicity for UVR-B-induced cataract in the guinea-pig. The pigmented guinea-pig is significantly less sensitive to UVR-B exposure than the pigmented rabbit and pigmented rat.

Protective effect of the thioltransferase gene on in vivo UVR-300 nm-induced cataract.

PURPOSE: To determine the protection factor (PF) for glutaredoxin-1 (Grx1) with regard to UVR-induced cataract by comparison of in vivo ultraviolet radiation (UVR) lens toxicity between double knockout Grx1⁻/⁻ and Grx1⁺/⁺ mice. METHODS: Twenty Grx1⁺/⁺ mice and 20 Grx1⁻/⁻ mice were unilaterally exposed in vivo to UVR for 15 minutes. Groups of four animals each received 0.0, 2.1, 2.9, 3.6, and 4.1 kJ/m(2) UVR-300 nm. At 48 hours after UVR exposure, light-scattering in the exposed and contralateral nonexposed lenses was measured quantitatively. Macroscopic lens changes were documented with dark-field illumination photography. RESULTS: UVR-300 nm induced subcapsular and cortical cataract in Grx1⁻/⁻ and Grx1⁺/⁺ mice. In both Grx1⁻/⁻ and Grx1⁺/⁺, the light-scattering intensified with increased in vivo exposure doses of UVR-300 nm. The intensity of forward light-scattering was higher in the lenses of Grx1⁻/⁻ mice than in the lenses of Grx1⁺/⁺ mice. The threshold dose for in vivo UVR-300 nm-induced cataract, expressed as MTD(2.3:16), was 3.8 in the Grx1⁺/⁺ group and 3.0 in the Grx1⁻/⁻ group, resulting in a PF of 1.3. CONCLUSIONS: The PF is an objective relative measure of protective properties. The Grx1 gene is associated with an in vivo PF of 1.3. This result signifies that the presence of the gene allows a 1.3 times longer in vivo exposure to UVR, at equivalent irradiance, than the absence of the gene before early-onset, UVR-induced cataract occurs. This finding indicates the important role of the Grx1 gene in the oxidation defense system of the lens.

Optical radiation and the eyes with special emphasis on children.

The Sun is the most abundant source of optical radiation for the child eye. New hand-held visible lasers are a threat to the child eye. Some scientific data suggest that near infrared radiation may cause cumulative damage in the ocular lens. The child eye usually is exposed to ambient solar radiation, gazing at the horizon. Ambient Sun ultraviolet radiation (UVR) exposure to the child is complex due to atmospheric scattering and strong dependence on background reflection. Solar exposure causes biological damage, only by photochemical mechanisms. UVR exposure to a child eye is mainly a threat to the anterior segment of the eye, but also age dependently to the retina. Above threshold exposure to UVR, for short delay onset of damage, causes a toxic reaction on the surface of the eye, snow blindness, and cataract. Sub-threshold daily exposure to UVR over decades is associated with several ocular surface pathologies and eye lid cancer. Visible radiation is a threat to the retina. A single above threshold exposure, for short delay onset of damage to the retina causes immediate photochemical Type II retinal damage, Sun blindness. A single exposure of the retina to a very high intensity laser beam may cause thermal or thermo-mechanical damage in the retina. In environments with high irradiance of optical radiation, the child eye should be protected. Legislation and public information is required for avoidance of damage from high intensity laser systems. More research is urgently needed to exclude the potential hazard of near infrared radiation.