Monitoring of central corneal thickness after phacoemulsification-comparison of statical and rotating Scheimpflug pachymetry, and spectral-domain OCT.

AIM: To explore the possibility of deploying three contactless devices (static and rotating Scheimpflug technology, spectral domain optical coherence tomography) for measuring central corneal thickness (CCT) in preoperative and postoperative examinations of cataract patients. METHODS: Totally 72 patients who had undergone surgery without complications were selected. The CCT was measured prior to the operation, as well as on the first, 5th-7th and 28th day following the operation using the Nidek NT 530-P, Sirius®, and Topcon OCT-2000 devices. RESULTS: A significant postoperative increase and subsequent decrease in CCT was identified with all three devices. The correlations were highly significant and thus reflect a very good degree of comparability at all times with the exception of the rotating Scheimpflug camera. The postoperative results from the latter differed significantly from the other devices. The correlations were Sirius/Topcon (P=0.010) and Sirius/Nidek (P<0.0005). No statistically significant difference could be identified in the comparison between Topcon and Nidek (P=0.056). CONCLUSION: All three devices are suitable for postoperative monitoring of CCT. The measurement results are only comparable to a limited extent and not interchangeable in the course of treating a single patient. This is due to the different imaging technology used in the devices and the resulting modalities for conducting the measurements.

UVR-B-induced NKR-1 Expression in Ocular Tissues is blocked by Substance P Receptor Antagonist Fosaprepitant in the Exposed as well as Unexposed Partner Eye.

Purpose: To investigate the effect of NKR-1 antagonists in an established UVR-B-induced cataract mouse model. Furthermore, to examine the expression of pro-inflammatory cytokines/chemokines in mouse eyes following unilateral UVR-B exposure.Methods: Mice received intraperitoneally injections of Fosaprepitant and Spantide I, before and after unilateral exposure to UVR-B. After day 3 and 7 post-exposure, ocular tissues were extracted for the detection of NKR-1 protein level by ELISA.Results: Pretreatment with Fosaprepitant decreases NKR-1 expression in exposed ocular tissues as well as in the unexposed lens epithelium compared to the saline group. Spantide I treatment showed a tendency of NKR-1 overexpression in ocular tissues.Conclusion: The clinically approved NKR-1 receptor antagonist Fosaprepitant decreases NKR-1 protein expression effectively not only in the exposed but also in the unexposed partner eye in a UVR-B irradiation mouse model. No effect was seen on the protein concentration of pro-inflammatory cytokines/chemokines in either eye.

Ultraviolet Radiation Exposure of One Eye Stimulates Sympathizing Expression of Neurokinin-1 Receptor but Not Monocyte Chemoattractant Protein-1 in the Partner Eye.

PURPOSE: To investigate the influence of unilateral ultraviolet radiation (UVR) exposure on the unexposed, partner eye in vivo. To characterize the immunological cross-talk between the eyes and verify a sympathizing reaction of the partner eye via a neurokinin-dependent signaling pathway of substance P and its neurokinin-1 receptor (NKR-1) and/or monocyte chemoattractant protein-1 (MCP-1). METHODS: C57BL/6 mice were unilaterally exposed in vivo to UVR-B to a 5-fold cataract threshold equivalent dose of 14.5 kJ/m2 with a UV irradiation Bio-Spectra system. The unexposed contralateral eye was completely shielded during irradiation. After 3 and 7 days post exposure, eyes were stained with fluorescence-coupled antibody for substance P NKR-1. The same was performed in control animals receiving only anesthesia but no UVR-B exposure. NKR-1 and MCP-1 levels in ocular tissue lysates were quantified by enzyme-linked immunosorbent assay. RESULTS: UVR-B induces NKR-1 upregulation after 3 and 7 days in the exposed and in the unexposed, contralateral mouse eye. NKR-1 protein level was upregulated in the exposed and contralateral iris/ciliary body complex, choroidea and in the contralateral retina as well as in the exposed cornea. MCP-1 levels were elevated in the exposed cornea, iris/ciliary body complex, and aqueous humor but not in contralateral ocular tissues. CONCLUSIONS: UVR-B exposure triggers NKR-1 upregulation not only in the exposed but also in the unexposed, partner eye in various ocular tissues. Following UVR-B exposure, MCP-1 protein levels are upregulated in the exposed eye, but the contralateral side remains unaffected.

Ionising radiation and lens opacities in interventional physicians: results of a German pilot study.

We assessed the feasibility of an epidemiological study on the risk of radiation-related lens opacities among interventional physicians in Germany. In a regional multi-centre pilot study associated with a European project, we tested the recruitment strategy, a European questionnaire on work history for the latter dosimetry calculation and the endpoint assessment. 263 interventional physicians and 129 non-exposed colleagues were invited. Questionnaires assessed eligibility criteria, risk factors for cataract, and work history relating to occupational exposure to ionising radiation, including details on type and amount of procedures performed, radiation sources, and use of protective equipment. Eye examinations included regular inspection by an ophthalmologist, digital slit lamp images graded according to the lens opacities classification system, and Scheimpflug camera measurements. 46 interventional (17.5%) and 30 non-exposed physicians (23.3%) agreed to participate, of which 42 and 19, respectively, met the inclusion criteria. Table shields and ceiling suspended shields were used as protective equipment by 85% and 78% of the interventional cardiologists, respectively. However, 68% of them never used lead glasses. More, although minor, opacifications were diagnosed among the 17 interventional cardiologists participating in the eye examinations than among the 18 non-exposed (59% versus 28%), mainly nuclear cataracts in interventional cardiologists and cortical cataracts in the non-exposed. Opacification scores calculated from Scheimpflug measurements were higher among the interventional cardiologists, especially in the left eye (56% versus 28%). Challenges of the approach studied include the dissuading time investment related to pupil dilatation for the eye examinations, the reliance on a retrospective work history questionnaire to gather exposure-relevant information for dose reconstructions and its length, resulting in a low participation rate. Dosimetry data are bound to get better when the prospective lens dose monitoring as foreseen by 2013 European Directives is implemented and doses are recorded.

Ultraviolet radiation exposure triggers neurokinin-1 receptor upregulation in ocular tissues in vivo.

The purpose of this study was to investigate the neurokinin receptor-1 (NKR-1) protein expression in ocular tissues before and after supra-cataract threshold ultraviolet radiation (UVR-B peak at 312 nm) exposure in vivo in a mouse model. Six-week-old C57Bl/6 mice were unilaterally exposed to a single (2.9 kJ/m2) and an above 3-fold UVR-B cataract threshold dose (9.4 kJ/m2) of UVR. UVR-exposure (λpeak = 312 nm) was performed in mydriasis using a Bio-Spectra exposure system. After latency periods of 3 and 7 days, eyes were fixed in 4% paraformaldehyde, embedded in paraffin, sectioned and stained with fluorescence coupled antibody for NKR-1 and DAPI for cell nuclei staining. Control animals received only anesthesia but no UVR-exposure. Cataract development was documented with a Leica dark-field microscope and quantified as integrated optical density (IOD). NKR-1 is ubiquitously present in ocular tissues. An above 3-fold cataract threshold dose of UV-radiation induced NKR-1 upregulation after days 3 and 7 in the epithelium and endothelium of the cornea, the endothelial cells of the iris vessels, the pigmented epithelium/stroma of the ciliary body, the lens epithelium, pronounced in the nuclear bow region and the inner plexiform layer of the retina. A significant upregulation of NKR-1 could not be provoked with a single cataract threshold dose (2.9 kJ/m2 UVR-B) ultraviolet irradiation. All exposed eyes developed anterior subcapsular cataracts. Neurokinin-1 receptor is present ubiquitously in ocular tissues including the lens epithelium and the nuclear bow region of the lens. UV-radiation exposure to an above 3-fold UVR-B cataract threshold dose triggers NKR-1 upregulation in the eye in vivo. The involvement of inflammation in ultraviolet radiation induced cataract and the role of neuroinflammatory peptides such as substance P and its receptor, NKR-1, might have been underestimated to date.

[Laser Iridotomy - In Cases of Acute Angle Closure Only?] / Laseriridotomie ­ nur bei akuter Engwinkelsituation?

The narrowing of the chamber angle-as a result of anatomic predispositions like high hyperopia or increasing lens thickness-poses the greatest risk for acute angle closure. A laser iridotomy counts as a standard procedure in cases of acute angle closure, whereas there are no coherent recommendations or guidelines for a prophylactic therapy. Modern imaging techniques, such as anterior segment optical coherence tomography or Scheimpflug photography, can give valuable information for the planning of treatment. This review presents traditional and modern imaging techniques and summarises recommendations for action in relation to recent publications.

Effect of Viscous Agents on Corneal Density in Dry Eye Disease.

PURPOSE: To investigate the effect of the viscous agents, hydroxypropyl methylcellulose (HPMC), carbomer, povidone, and a combination of HPMC and povidone on corneal density in patients with dry eye disease. METHODS: In total, 98 eyes of 49 patients suffering from dry eye and 65 eyes of 33 healthy age-matched individuals were included in this prospective, randomized study. Corneal morphology was documented with Scheimpflug photography and corneal density was analyzed in 5 anatomical layers (epithelium, bowman membrane, stroma, descemet's membrane, and endothelium). Corneal density was evaluated for the active ingredients HPMC, carbomer, povidone, and a combination of HPMC and povidone as the viscous agents contained in the artificial tear formulations used by the dry eye patients. Data were compared to the age-matched healthy control group without medication. RESULTS: Corneal density in dry eye patients was reduced in all 5 anatomical layers compared to controls. Corneal density was highest and very close to control in patients treated with HPMC containing ocular lubricants. Patients treated with lubricants, including carbomer as the viscous agent displayed a significant reduction of corneal density in layers 1 and 2 compared to control. CONCLUSION: HPMC containing ocular lubricants can help to maintain physiological corneal density and may be beneficial in the treatment of dry eye disease.

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.

Cataract prevalence and prevention in Europe: a literature review.

This literature review is aimed at the evaluation of the potential for cataract prevention in Europe. It was performed using PubMed with Mesh and free-text terms. Studies included were (i) performed on a population of Caucasian origin at an age range of 40-95 years, (ii) cataract was clinically verified, (iii) drug record of prescriptions, their indication, a record of every diagnosis, dosage and quantity of prescribed medicine were available, (iv) sample size >300 and (v) published between 1990 and 2009. The results of 29 articles were reviewed. Former [3.75 (2.26-6.21)] or current smoking [2.34 (1.07-5.15)], diabetes of duration >10 years [2.72 (1.72-4.28)], asthma or chronic bronchitis [2.04 (1.04-3.81)], and cardiovascular disease [1.96 (1.22-3.14)] increased the risk of cataract. Cataract was more common in patients taking chlorpromazine during ≥90 days with a dosage ≥300 mg [8.8 (3.1-25.1)] and corticosteroids >5 years [3.25 (1.39-7.58)] in a daily dose >1600 mg [1.69 (1.17-2.43)]. Intake of a multivitamin/mineral formulation [2.00 (1.35-2.98)] or corticosteroids [2.12 (1.93-2.33)] also increased the risk of cataract. Corticosteroids applied orally [3.25 (1.39-7.58)], parenteral [1.56 (1.34-1.82)] or inhalational [1.58 (1.46-1.71)] lead to cataract more frequently than those applied topically: nasal [1.33 (1.21-1.45)], ear [1.31 (1.19-1.45)] or skin [1.43 (1.36-1.50)]. Outpatient cataract surgery was negatively associated with total cataract surgery costs, and chlorpromazine, corticosteroids and multivitamin/mineral formation increase the risk of posterior subcapsular cataract dependent on dose, treatment application and duration. This review presented a comprehensive overview of specific and general cataract risk factors and an update on most recent experimental studies and randomized control trials directed at cataract prevention.

Bilateral cataract induced by unilateral UVR-B exposure -- evidence for an inflammatory response.

PURPOSE: To investigate whether unilateral in vivo UVR-B exposure of one eye affects the fellow eye in a co-cataractogenic, sympathetic reaction and to determine whether an inflammatory response could be involved in the pathogenesis. METHODS: C57BL/6 mice were unilaterally exposed in vivo to UVR-B for 15 min. In the group of 24 animals each received 0×/2×/3×/or 4× cataract threshold equivalent dose. Following 48-hr UVR-B exposure, cataract morphology was documented in dark-field illumination photography, and light scattering was quantified, in both lenses in vitro. Serum levels of pro-inflammatory cytokines IL-1ß, IL-6 and TNF-α were analysed with ELISA. Immunohistochemistry was performed for inflammatory infiltration in exposed and contralateral eyes. RESULTS: UVR-B exposure induced cataract in all exposed lenses. There was additionally a significant UVR dose-dependent increase in light scattering in the lenses of the non-exposed fellow eye. Inflammatory infiltration was detected immunohistochemically in the anterior segment of both eyes. IL-1ß serum concentration increased with increasing UVR-B exposure dose. There was a similar trend for serum IL-6 but not for TNF-α. CONCLUSION: Unilateral UVR-B exposure to one eye is associated with intraocular inflammation and an increase in lens light scattering also in the unexposed, fellow eye. A resulting systemic inflammatory response might be mediated by IL-1ß and possibly IL-6. The finding that an inflammatory response may play a role in UVR-B-induced cataract development might initiate new strategies in the prevention of the disease.

Localisation and significance of in vivo near-infrared autofluorescent signal in retinal imaging.

AIM: To evaluate near-infrared (NIR) autofluorescence (AF) in patients with geographic atrophy (GA) secondary to age-related macular degeneration and to investigate the origin of the signal by in vivo and histological analysis in rats and in a human donor eye. METHODS: Confocal scanning laser ophthalmoscopy in vivo imaging, including blue (excitation: 488 nm, emission 500-700 nm) and NIR (excitation: 790 nm, emission >810 nm) AF was performed in 21 eyes of 18 GA patients. Pigmented and albino rats underwent with the same device both in vivo and post-mortem imaging. For the latter, cryostat prepared retinal cross-sections were imaged using an additional customised magnification lens. Finally, cross-sections of a 49-year old human donor eye were recorded. RESULTS: Atrophic areas in GA were characterised by low NIR AF intensities. In the junctional zone of atrophy, focal areas of increased intensity were seen which appeared to seldom correlate to blue AF findings. Confocal live scanning in pigmented rats identified the maximum of the NIR AF signal in the outer retina, with histological confirmation of the signal origin localised to the retinal pigment epithelium and sclera in both animals and human donor eye. No NIR AF was found in the retina of young non-pigmented rats. DISCUSSION: This study further underscores the assumption that melanin is the main source of NIR AF in the healthy retina. Increased NIR AF intensities in the junctional zone in GA may represent accumulation of melanolipofuscin, which may reflect disease activity and thus may allow for early identification of patients at high-risk of GA enlargement.

Femtosecond lentotomy: generating gliding planes inside the crystalline lens to regain accommodation ability.

Based on Helmholtz Theory for accommodation the increasing sclerosis of lens nucleus and cortex is the main cause for the developments of presbyopia. Existing therapies, however, do not reverse the stiffness of the crystalline lens and thus do not regain real accommodation ability. A new approach to restore the flexibility of the lens could be realized by photodisruption using ultrafast laser pulses. This process, known as fs-lentotomy, was used to create micro-incisions which act as gliding planes inside the crystalline lens without opening the eye globe.

Absence of glutaredoxin1 increases lens susceptibility to oxidative stress induced by UVR-B.

We investigated if the absence of glutaredoxin1, a critical protein thiol repair enzyme, increases lens susceptibility to oxidative stress caused by in vivo exposure to ultraviolet radiation type B (UVR-B). Glrx(-/-) mice and Glrx(+/+) mice were unilaterally exposed in vivo to UVR-B for 15 min. Groups of 12 animals each received 4.3, 8.7, and 14.5 kJ/m(2) respectively. 48 h post UVR-B exposure, the induced cataract was quantified as forward lens light scattering. Cataract morphology was documented with darkfield illumination photography. Glutathione (GSH/GSSG) content was analyzed in Glrx(-/-) and Glrx(+/+) lenses. UVR-B exposure induced anterior sub-capsular cataract (ASC) in Glrx(-/-) and Glrx(+/+) mice. In Glrx(-/-) lenses the opacities extended further towards the lens equator than in wild type animals (Glrx(+/+)). Lens light scattering in Glrx(-/-) mice was increased in all dose groups compared to lenses with normal glutaredoxin1 function. The difference was more pronounced with increasing exposure dose. Lens sensitivity for UVR-B induced damage was significantly higher in Glrx(-/-) lenses compared to Glrx(+/+) lenses. The Glrx gene provides a 44% increase of protection against close to threshold UVR-B induced oxidative stress compared to the absence of the Glrx gene. In conclusion, the absence of glutaredoxin1 increases lens susceptibility to UVR-B induced oxidative stress in the mouse.

Femtosecond laser induced flexibility change of human donor lenses.

BACKGROUND: According to the Helmholtz theory of accommodation the loss of accommodation amplitude is caused by the growing sclerosis of the crystalline lens, whereas the ciliary muscle and the lens capsule are mainly uneffected by age. A permanent treatment method for presbyopia which offers a dynamic accommodation ability is a recent field of study. The concept followed in this paper uses femtosecond laser pulses to potentially overcome the loss of deformation ability of the crystalline lens by creating gliding planes inside the lens tissue to improve its flexibility. METHODS: The aim of the study is to show that the flexibility of human donor lenses can be increased by applying tightly focused near infrared femtosecond laser pulses into the lens tissue. Thereby the tissue is separated by the photodisruption effect. A certain pattern of gliding planes is cut inside the tissue of 41 human donor lenses and the deformation ability of the lenses are compared using the Fisher spinning test before and after laser treatment. RESULTS: The laser treatment results in an increased deformation ability of the crystalline lens. The lens a-p thickness increases on average by 97 microm+/-14 microm after the treatment. The Fisher spinning test shows an increase of 16% in deformation ability of the lens at a rotational speed of 1620 rpm. CONCLUSION: The creation of gliding planes with a fs laser inside the crystalline lens tissue can change the deformation ability of the lens. This might be an indication for a possible method to treat presbyopia in future.

Photography of the anterior eye segment according to Scheimpflug's principle: options and limitations - a review.

Scheimpflug photography and densitometric image analysis are very precise techniques for light scattering measurement and biometry in the anterior segment of the eye. They provide reproducible data on the characteristics of the anterior eye segment in clinical and experimental studies and the set of data obtained allows discrimination of light scattering changes because of ageing, disease or toxic effects. The techniques can also be used to determine no-effect levels or maximally tolerable dosages of physical and chemical noxious factors. Several Scheimpflug cameras have been marketed, but the only cameras commercially available today are the Nidek EAS 1000 and the Oculus Pentacam. This review outlines the development of the technique and its introduction into ophthalmology. Furthermore, the application of the technique in clinical and experimental ophthalmology as well as in ocular toxicology are presented and discussed.

In vivo application and imaging of intralenticular femtosecond laser pulses for the restoration of accommodation.

PURPOSE: According to the Helmholtz theory of accommodation, one major cause of the development of presbyopia is the increasing sclerosis of the crystalline lens. One concept for regaining the elasticity of the sclerosing lens is intralenticular treatment by femtosecond laser pulses. METHODS: The feasibility of applying and imaging in vivo microincisions by femtosecond laser pulses was evaluated in five rabbit lenses with a new high repetition rate (100 kHz) femtosecond laser unit. The treated eyes were monitored using optical coherence tomography (OCT) and Scheimpflug imaging for localizing and studying the tissue effects of the incisions. The rabbits were investigated preoperatively, immediately postoperatively, and 14 days after treatment. RESULTS: The procedure, termed femtosecond-lentotomy, was successfully applied to the left lens of each rabbit. The laser microincisions within the crystalline lens were detectable with OCT and Scheimpflug imaging, which emphasizes the integral role these technologies play in targeting and characterizing postoperative tissue effects. The imaging within the lens showed a progressive fading of the incisional opacities generated by the femtosecond laser after 14 days with no detectable cataract formation. CONCLUSIONS: It is possible to create microincisions inside the crystalline lens within an acceptably short treatment time (<30 seconds). The 14-day follow-up did not show undesirable side effects, such as cataract formation, after intralenticular laser treatment.

Retinal safety of a new fluoroquinolone, pradofloxacin, in cats: assessment with electroretinography.

PURPOSE: To investigate the safety of a new fluoroquinolone, pradofloxacin, on the cat retina using electroretinogram. METHODS: Ganzfeld ERGs were recorded in 40 cats treated orally for 23 days in 4 groups: CTRL (n = 9): placebo-vehicle; PRADO30 (n = 10): pradofloxacin 30 mg/kg/day; PRADO50 (n = 14): pradofloxacin 50 mg/kg/day; and ENRO30 (n = 7): enrofloxacin at toxic doses of 30 mg/kg/day. ERG was performed before treatment and once weekly during the treatment period. An extended ISCEV protocol with addition of 8 steps of increasing luminance in dark adapted condition was carried out to assess: V (max) (saturated scotopic b-wave amplitude) and k (luminance inducing V (max)/2). OCT and retinal histological changes were also investigated. RESULTS: Pradofloxacin showed no effects in respect to rod b-wave, V (max), k and maximum scotopic a-wave (P > 0.05). Oscillatory potentials, cone ERG and flicker were also unaltered (P > 0.05). Rod b-wave was undetectable after treatment in ENRO30 group, V (max) was reduced to 10.5% of the baseline (P < 0.05), accompanied by an increase of k by 1 log cd s/m(2) (P < 0.05). Oscillatory potentials, cone b-wave amplitude and 30 Hz flicker amplitude were reduced to 8.3%, 58.9% and 37.4% of the baseline, respectively (P < 0.05). Effects were also seen in OCT and retinal histology starting within one week after the start of treatment and thereafter remaining stable. CONCLUSION: Pradofloxacin at 6 and 10 times the recommended doses was shown to have no retinal toxic effects in cats, neither on rod or cone function with ERG.

Dose dependent cataractogenesis and Maximum Tolerable Dose (MTD(2.3:16)) for UVR 300 nm-induced cataract in C57BL/6J mice.

The purpose of the present study was to investigate the in vivo dose response function for UVR 300 nm-induced cataract in the C57BL/6J mouse lens and to establish a cataract threshold estimate expressed as Maximum Tolerable Dose (MTD(2.3:16)) for UVR 300 nm-induced cataract in the C57BL/6J mouse lens. Knowledge of the MTD(2.3:16) in the C57BL/6J mouse will permit quantitative in vivo comparison of UVR-B threshold sensitivity of knockout mice, e.g. animals deficient in key antioxidative enzymes or mice suffering from genetically predetermined eye disease, to wild type animals. Eighty C57BL/6J mice were divided into four dose groups. The animals were exposed unilaterally to 0, 2, 4, or 8 kJ/m(2) UVR 300 nm for 15 min (n=20). The radiation output of the UVR-source had lambda(max) at 302.6 nm with 5 nm full width at half maximum. Two days after exposure cataract was quantified as forward lens light scattering intensity in the exposed and the contralateral non-exposed lens. Morphological lens changes were documented using grid and dark field illumination photography. MTD(2.3:16) was estimated from the forward light scattering measurements. Two days after exposure mainly anterior subcapsular but also cortical and nuclear cataract developed in lenses that had received 2, 4, and 8 kJ/m(2) UVR 300 nm. Forward light scattering intensity increased with increasing UVR 300 nm dose. MTD(2.3:16) for the mouse lens was estimated to 2.9 kJ/m(2) UVR 300 nm. Lens light scattering intensity in the C57BL/6J mouse lens increases with UVR 300 nm in vivo dose in the range 0-8 kJ/m(2). The MTD(2.3:16) of 2.9 kJ/m(2) in the C57BL/6J mouse lens determined here, is essential to quantify and compare in vivo the impact of genetic modulation on lens susceptibility to oxidative stress and plan dose-ranges in future investigations of UVR 300 nm-induced cataract pathogenesis.

Light scattering in the C57BL/6 mouse lens.

PURPOSE: To characterize inherent light scattering in the C57BL/6 mouse lens. METHODS: Lenses from 20 6-week-old female C57BL/6 mice were extracted from freshly enucleated globes and microsurgically cleaned of remnants of the ciliary body. Lens light scattering was measured quantitatively with a light dissemination meter (LDM). Morphological properties of the mouse lenses were documented using grid- and dark-field illumination photography. Analysis of variance was performed to establish variance for animals, variance between left and right eyes and variance for measurements. RESULTS: Average inherent light scattering in the C57BL/6 mouse lens is 0.16 +/- 0.02 tEDC (transformed equivalent diazepam concentration). The mean size of a mouse lens at 6 weeks is 1.9 mm in diameter. Two lenses featured pre-existing cortical lens opacities. Variance for animals was assessed to be 7.9 10(- 4) tEDC(2), variance for measurements was 1.6 10(- 4) tEDC(2), and variance between left and right eyes was 8.8 10(- 4) tEDC(2). The tolerance limit for non-pathological light scattering was determined to 0.26 tEDC. No significant difference in light scattering between left and right mouse lenses was found. The minimum number of C57BL/6 mice required for detection of a 10% experimentally induced change in light scattering intensity was estimated to be 50 for independent group experiments and 25 for paired design experiments. CONCLUSIONS: The C57BL/6 mouse is a suitable animal in which to conduct experiments on light scattering or cataractogenesis with high precision at reasonable sample sizes. Before including C57BL/6 mice into a study on cataractogenesis, pre-existing lens opacities such as congenital cataract must be excluded.

UVR-B induced cataract development in C57 mice.

The evolution of the morphological appearance and intensity of light scattering in C57 mice lenses after exposure to ultraviolet radiation type B (UVR-B) was investigated. A total of 80, 6-week-old female C57BL/6 mice were divided into four groups (n=20). One eye in each animal was exposed in vivo to UVR-B in the 300 nm wavelength region (UVR-B-300 nm) to a dose of 5 kJm(-2) for 15 min. The radiation output had lambda(max) at 302 nm with 5 nm [FWHM]. The animals were consecutively sacrificed at 1, 2, 4 and 8 days after the exposure. Macroscopic lens changes were documented using grid- and dark field illumination photography. Light scattering in the exposed and contralateral not exposed lens was measured quantitatively. Morphological lens changes were documented using grid- and dark field illumination photography. In vivo exposure to UVR-B-300 nm induced subcapsular cataract in all exposed lenses and occasionally cortical and nuclear cataract at all investigated time points. Exposed lenses scattered light significantly higher on all investigated days compared to contralateral non-exposed lenses. A transient increase of light scattering peaking at day 2 in exposed as well as in contralateral not exposed lenses was identified. Light scattering of the lenses varies with latency time after exposure. A dose of 5 kJm(-2) UVR-B-300 nm induces light scattering in C57 mice lenses. The increase has a transient peak at 2 days after exposure. The variation of light scattering among days 1, 2, 4, and 8 indicates a dynamic change of scattering characteristics in the mouse lens following unilateral in vivo exposure to 5 kJm(-2) UVR-B-300 nm.