Unlocking the Use of LiCl as an Inexpensive Salt for Lithium-Ion Batteries with a Novel Anion Receptor.

Lithium chloride (LiCl) is an inexpensive and environmentally friendly salt abundant in the ocean. However, the insolubility of LiCl in conventional electrolyte solvents prevents the practical use of LiCl for lithium-ion batteries. Here, we report a novel method to increase the solubility of LiCl in a conventional electrolyte. The solubility of LiCl in ethylene carbonate (EC)/dimethyl carbonate (DMC) (1/1, v/v) is about quadrupled by adding a small amount of anion receptor with two urea moieties as recognition sites connecting with an ether chain. Anion receptor is an organic molecule that can associate with anions. Our anion receptor is able to associate with chloride anion. The ionic conductivity of LiCl in EC/DMC increased from 0.023 mS cm-1 (without an anion receptor) to 0.075 mS cm-1 (with a 0.05 M anion receptor). The electrolyte in the presence of a 0.05 M receptor exhibits higher ionic conductivity, rate capability, and cyclability than the electrolyte without the receptor.

Highly soluble bisurea derivatives for anion recognition.

Highly soluble bisurea derivatives having 1,2-phenoxyethane (receptors 2) and 1,2-ethoxyethane (3) moieties as spacer groups were designed and prepared based on previously reported receptors with the 2,2'-binaphthyl group as a spacer (1). The receptors can be prepared in fewer steps from commercially available starting materials. The solubilities and anion recognition abilities were evaluated by UV-vis and NMR spectral methods. Receptors 2 and 3 bearing a flexible linker showed good solubilities in common organic solvents such as CHCl3, MeCN, 2-butanone, toluene, and THF. Although the anion recognition abilities of receptors 2 and 3 were lower than those of receptors 1, the greatly improved solubilities of receptors 2 and 3 allow the association of anions under more concentrated conditions for the solubilisation of salts such as lithium chloride in organic solvents.

Binocular visual function after staged implantation of extended-depth-of-focus intraocular lens targeting emmetropia and -0.5 diopter: A prospective comparison.

The prospective comparative case series aimed to evaluate the binocular uncorrected visual acuities (BUCVAs) after staged implantations of extended-depth-of-focus intraocular lenses (EDOF IOLs) targeting emmetropia and -0.5 diopter (D). Diffractive EDOF IOLs with an add power of +1.75 D were implanted in the first eyes targeting emmetropia or -0.5 D according to the patients' preferences, then the targets for the second eyes were determined 1 week or longer after the implantation. IOL powers were determined with the SRK/T formula. Consequently, the subjects were divided into 3 groups: those with emmetropia targeted bilaterally (group EE, 22 patients), those with -0.5 D targeted bilaterally (group MM, 21 patients), and those with monovision of emmetropia and -0.5 D (group EM, 21 patients). Manifest refraction spherical equivalent (MRSE), BUCVA from 0.3 to 5 meters, spectacle use, and questionnaire regarding photic symptoms and patient satisfaction were assessed 3 months postoperatively. No significant differences were seen in the mean BUCVAs at any distance (P > 0.23), spectacle use (P = 0.13), or photic symptoms and patient satisfaction (P>0.65). When the EE and MM groups were assigned based on the MRSE, the EE group was better at 5 m (P = 0.005) while the MM group at 0.5 m (P = 0.031). The effect of different targeted refractions was not identified due to insufficient accuracy in the use of the SRK/T power calculation.

Binocular Visual Function With Staged Implantation of Diffractive Multifocal Intraocular Lenses With Three Add Powers.

PURPOSE: To evaluate the binocular visual function and depth of focus after staged implantation of diffractive multifocal intraocular lenses (MIOLs) with 3 different add powers following cataract removal. DESIGN: Prospective comparative case series. METHODS: Setting: Institutional. STUDY POPULATION: Both eyes of 56 patients that underwent staged implantation of bifocal IOLs. INTERVENTION: In the first eye, MIOLs with a +4.0-diopter (D) add power were implanted. Based on outcomes at 1 week postoperatively and patient preference for near vision, 1 of 3 near add powers-+4.0 D (group MM), +3.25 D (group ML), or +2.75 D (group MK)-was implanted in the fellow eye. MAIN OUTCOME MEASURE(S): Three months postoperatively, the binocular uncorrected and distance-corrected visual acuities (BUCVA and BDCVA, respectively) at 5.0, 1.0, 0.5, 0.4, and 0.3 meters; binocular defocus curves; contrast sensitivity; and near stereopsis were measured. RESULTS: The MM, ML, and MK groups included 21, 18, and 17 patients, respectively. The mean BUCVA in the MM group was significantly (P = .003) worse than that in the MK group at 0.5 meter. The BDCVAs at 0.5 meter in the ML and MK groups were significantly (P < .02) better than that in the MM group. The defocus curves with the -2.0 D refraction differed significantly (P < .001) between the MM and MK groups. The binocular contrast sensitivity and stereopsis values did not differ significantly. CONCLUSIONS: Staged implantation of different add powers obtained better binocular intermediate visual acuity without degradation of visual function.

Self-Healing Micellar Ion Gels Based on Multiple Hydrogen Bonding.

Ion gels, composed of macromolecular networks filled by ionic liquids (ILs), are promising candidate soft solid electrolytes for use in wearable/flexible electronic devices. In this context, the introduction of a self-healing function would significantly improve the long-term durability of ion gels subject to mechanical loading. Nevertheless, compared to hydrogels and organogels, the self-healing of ion gels has barely investigated been because of there being insufficient understanding of the interactions between polymers and ILs. Herein, a new class of supramolecular micellar ion gel composed of a diblock copolymer and a hydrophobic IL, which exhibits self-healing at room temperature, is presented. The diblock copolymer has an IL-phobic block and a hydrogen-bonding block with hydrogen-bond-accepting and donating units. By combining the IL and the diblock copolymer, micellar ion gels are prepared in which the IL phobic blocks form a jammed micelle core, whereas coronal chains interact with each other via multiple hydrogen bonds. These hydrogen bonds between the coronal chains in the IL endow the ion gel with a high level of mechanical strength as well as rapid self-healing at room temperature without the need for any external stimuli such as light or elevated temperatures.

Safety and reliability of femtosecond laser-assisted cataract surgery for Japanese eyes.

PURPOSE: To assess the safety and efficacy of femtosecond laser-assisted cataract surgery (FLACS) in Japanese eyes. STUDY DESIGN: Retrospective case series. METHODS: The clinical records of 529 consecutive eyes of 312 Japanese patients who underwent FLACS from 2013 to 2016 were reviewed. The completion rates of anterior capsulotomy and corneal incisions using the femtosecond laser (LenSx, Alcon) and the number of attempts to achieve secure docking between the cornea and laser system were recorded. The uncorrected and corrected distance visual acuities (VAs) and uncorrected and distance-corrected near VAs 1 week postoperatively were evaluated. RESULTS: Anterior capsulotomies were completed in 98.7% of eyes. The corneal incisions were incomplete in 8.3%, which included eyes with arcus senilis and neovascularization. The mean corneal endothelial cell reduction rate was 5.5%. Multiple docking attempts were required in 22.9% of eyes, while canthotomy was performed in two eyes. The postoperative VAs were favorable. CONCLUSION: FLACS was safe and reliable in Japanese eyes. Further improvements in docking are required to accommodate small corneas and narrow palpebral spaces.

Angiopoietin-like Protein 2 Is a Multistep Regulator of Inflammatory Neovascularization in a Murine Model of Age-related Macular Degeneration.

Choroidal neovascularization (CNV) is a pathogenic process of age-related macular degeneration, a vision-threatening disease. The retinal pigment epithelium and macrophages both influence CNV development. However, the underlying mechanisms remain obscure. Here, we focus on Angptl2 (angiopoietin-like protein 2), a cytokine involved in age-related systemic diseases. Angptl2 was originally identified as an adipocytokine and is also expressed in the eye. Using a laser-induced CNV model, we found thatAngptl2KO mice exhibited suppressed CNV development with reduced macrophage recruitment and inflammatory mediator induction. The mediators monocyte chemotactic protein-1, interleukin-1ß (Il-1ß),Il-6, matrix metalloprotease-9 (Mmp-9), and transforming growth factor-ß1 (Tgf-ß1) that were up-regulated during CNV development were all suppressed in the retinal pigment epithelium-choroid of CNV models generated in theAngptl2KO mice. Bone marrow transplantation using wild-type and KO mice suggested that both bone marrow-derived and host-derived Angptl2 were responsible for macrophage recruitment and CNV development. Peritoneal macrophages derived fromAngptl2KO mice expressed lower levels of the inflammatory mediators. In the wild-type peritoneal macrophages and RAW264.7 cells, Angptl2 induced the mediators via integrins α4 and ß2, followed by the downstream activation of NF-κB and ERK. The activation of NF-κB and ERK by Angptl2 also promoted macrophage migration. Therefore, Angptl2 from focal tissue might trigger macrophage recruitment, and that from recruited macrophages might promote expression of inflammatory mediators including Angptl2 in an autocrine and/or paracrine fashion to facilitate CNV development. Angptl2 might therefore represent a multistep regulator of CNV pathogenesis and serve as a new therapeutic target for age-related macular degeneration.

[Clinical Results of Diffractive Multifocal Intraocular Lens Implantation after Laser In Situ Keratomileusis].

PURPOSE: To evaluate the visual performance in eyes with diffractive intraocular lenses (IOLs) after laser in situ keratomileusis (LASIK). METHODS: This single-center retrospective study evaluated eyes that had diffractive multifocal IOL implantation after previous LASIK or not treated with LASIK (controls). The outcomes' measures were the visual acuities (VAs) at distance and near, spherical equivalent (SE) and contrast sensitivity at one month postoperatively. RESULTS: The study evaluated 40 eyes of 33 patients. The mean uncorrected logMAR VAs were -0.05 ± 0.13/0.00 ± 0.14 (LASIK group/control group) at distance and 0.10 ± 0.13/0.16 ± 0.18 at near. There was no statistically significant difference between the 2 groups at the VAs. The SE of the LASIK group was -0.06 ± 0.39 D, significantly lower than the control group (0.22 ± 0.45 D) (p < 0.05). The contrast sensitivity of the LASIK group at high spatial frequency was lower than the control group (p < 0.05). CONCLUSION: After LASIK, the diffractive multifocal IOL provided good uncorrected distance and near VAs. However, decrease in contrast sensitivity should be considered.

[Clinical Results of Tinted Aspherical Multifocal IOL with +2.5 Diopter Near Add Power SN6AD2 (SV25T0)].

PURPOSE: To evaluate the efficacy and safety of a newly developed diffractive multifocal intraocular lens (IOL) with +2.5 diopter near add power (SN6AD2, Alcon), whose theoretical distance for near focus is 50 cm. METHODS: This study included 128 eyes of 64 patients (23 men and 41 women, average age: 66.7 ± 7.2 years) following cataract removal at Tokyo Dental College Suidobashi Hospital and Hayashi Eye Hospital. Visual acuities (VAs) at distance, 1 m, 50 cm and 40 cm, and questionnaires were evaluated until 1 year postoperatively. RESULTS: At 1 year postoperatively, mean bilateral logMAR VAs were uncorrected -0.09 (5 m), 0.01 (1 m), 0.07 (50 cm), 0.18 (40 cm), distance corrected 0.01 (1 m), 0.08 (50 cm), 0.19 (40 cm), best corrected -0.17 (5 m), 0.00 (50 cm). From the patient's questionnaires, light or moderate glare was noticed in 17.5%, 4.8%, light or moderate halo was notice in 19.0%, 4.8% of the total patients. CONCLUSION: This IOL provides good distance to intermediate VAs and better near VA compared to monofocal IOL.

[Clinical results of tinted aspheric multifocal toric intraocular lens (SND1T3, SND1T4, SND1T5, SND1T6) for eyes following cataract extraction].

PURPOSE: The efficacy and safety of tinted aspheric multifocal toric intraocular lens (IOL) (SND1T3, SND1T4, SND1T5, SND1T6 : Alcon) were evaluated in 130 eyes of 65 patients following cataract removal. METHODS: Visual acuities (VAs) at distance, near (40 cm) and intermediate (50 cm, 1 m), IOL rotation, contrast sensitivity, spectacle usage and glare/halo were examined up to 1 year postoperatively. RESULTS: The mean bilateral uncorrected distance VA was -0.04 ± 0.10 logMAR, near VA was 0.00 ± 0.11 logMAR, intermediate VA at 50 cm was -0.00 ± 0.11 logMAR, intermediate VA at 1 m was 0.11 ± 0.15 logMAR. IOL rotation was 5.73 ± 4.36 degrees, photopic contrast sensitivities were within normal range, and 76.9% of the patients did not require any spectacles. None of the patients complained of either serious glare or halo. CONCLUSION: The multifocal toric IOL provides better VA from distance to near at 40 cm.

Blue light-induced inflammatory marker expression in the retinal pigment epithelium-choroid of mice and the protective effect of a yellow intraocular lens material in vivo.

Oxidative stress in the retinal pigment epithelium (RPE) is a well-accepted pathogenic change in vision-threatening diseases such as age-related macular degeneration. One source of oxidative stress is excessive light exposure, which causes excessive activation of the visual cycle. Because short wavelength light (blue light) has more energy, it is reported to be more harmful to photoreceptor cells than the other wavelengths of light. However, the biological effect of blue light in the RPE of living animals and the protective effect of a yellow intraocular lens (IOL) material that blocks blue light is still obscure. Therefore, we compared the pathogenic effect in the RPE-choroid complexes of mice exposed to light in a box made of a clear or a yellow IOL material. We measured the level of reactive oxygen species (ROS) using 2', 7'-dichlorodihydrofluorescein diacetate, the mRNA levels of inflammatory cytokines and a macrophage marker by real-time polymerase chain reaction, and the protein level of monocyte chemotactic protein-1 (MCP-1) by ELISA. The ROS level after light exposure was suppressed in the RPE-choroids of light-exposed mice in the yellow IOL material box. In parallel, all the inflammatory cytokines that we measured and a macrophage marker were also suppressed in the RPE-choroids of light-exposed mice in the yellow IOL material box. Therefore, a yellow IOL material suppressed, and thus blue light exacerbated, the increase in the ROS level and inflammatory cytokine expression as well as macrophage recruitment in the RPE-choroid in vivo after light exposure.

Disruption of cell-cell junctions and induction of pathological cytokines in the retinal pigment epithelium of light-exposed mice.

PURPOSE: To elucidate the influences of light exposure on the retinal pigment epithelium (RPE) in vivo that may be involved in the pathogenesis of AMD. METHODS: Six- to 7-week-old BALB/c mice were exposed to light at 2000 lux for 3 hours. Flat-mount RPE samples were immunostained with anti-ZO-1 antibody for evaluating tight junction, anti-N-cadherin, and anti-ß-catenin antibodies for adherens junction, and stained with phalloidin for actin cytoskeleton. The reactive oxygen species (ROS) level was measured using DCFH-DA; Rho-associated coiled-coil forming kinase (ROCK) activity was by ELISA. Cytokine expression was analyzed by real-time RT-PCR and/or ELISA in the RPE-choroid, and macrophage recruitment was by real-time RT-PCR and immunohistochemistry. Either an antioxidant, N-Acetyl-L-cysteine (NAC), or a ROCK inhibitor, Y-27632, were administered to analyze the roles of ROS and ROCK activation, respectively. RESULTS: Light exposure disrupted staining patterns of tight junctions, adherens junctions, and actin cytoskeleton in the RPE, where ROS was elevated. However, NAC treatment avoided the RPE changes, reducing ROS. ROCK activity increased after light exposure was suppressed by NAC, and the structural disruptions were suppressed by Y-27632. The levels of MCP-1, CCL11, and IL-6 increased after light exposure were suppressed by NAC. Light-induced MCP-1 and IL-6 were suppressed by Y-27632. Macrophage recruitment after light exposure was also suppressed either by NAC or Y-27632. CONCLUSIONS: Light exposure induced ROS and Rho/ROCK activation, which caused disruption of cell-cell junctions (tight junctions and adherens junctions) and actin cytoskeleton, the RPE's barrier structure, and induced AMD-associated pathological changes in the RPE-choroid.

Cyclooxygenase inhibitor improved an exudative lesion of choroidal neovascularization in age-related macular degeneration.

PURPOSE: To report a case in which a nonselective cyclooxygenase (COX) inhibitor improved an exudative lesion in age-related macular degeneration. METHODS/RESULTS: A 64-year-old man had a complaint of metamorphopsia in the left eye. Visual acuity was 0.5 in the left eye. Fluorescein angiography and indocyanine angiography showed juxtafoveal occult choroidal neovascularization (CNV) in the left eye, and pegaptanib sodium 0.3 mg was administered once every 6 weeks. After 4 months, visual acuity improved to 0.8. After 8 months follow-up, optical coherence tomography (OCT) showed subretinal fluid (SRF) and retinal pigment epithelium (RPE) irregularity. Visual acuity was 0.4. We recommended further pegaptanib sodium injections, but the patient did not consent to the treatment. Onset of cellulitis of the left toe occurred 1 week before the scheduled visit after 9 months. The patient was treated with loxoprofen sodium (nonselective COX inhibitor) and cefdinir for 7 days. At 2 weeks after onset of cellulitis, SRF had disappeared and OCT showed improvement of RPE irregularity. CONCLUSIONS: A COX inhibitor had an effect on vascular permeability in CNV and may have improved exudative changes.

Neuroprotective response after photodynamic therapy: role of vascular endothelial growth factor.

BACKGROUND: Anti-vascular endothelial growth factor (VEGF) drugs and/or photodynamic therapy (PDT) constitute current treatments targeting pathological vascular tissues in tumors and age-related macular degeneration. Concern that PDT might induce VEGF and exacerbate the disease has led us to current practice of using anti-VEGF drugs with PDT simultaneously. However, the underlying molecular mechanisms of these therapies are not well understood. METHODS: We assessed VEGF levels after PDT of normal mouse retinal tissue, using a laser duration that did not cause obvious tissue damage. To determine the role of PDT-induced VEGF and its downstream signaling, we intravitreally injected a VEGF inhibitor, VEGFR1 Fc, or a PI3K/Akt inhibitor, LY294002, immediately after PDT. Then, histological and biochemical changes of the retinal tissue were analyzed by immunohistochemistry and immunoblot analyses, respectively. RESULTS: At both the mRNA and protein levels, VEGF was upregulated immediately and transiently after PDT. VEGF suppression after PDT resulted in apoptotic destruction of the photoreceptor cell layer in only the irradiated area during PDT. Under these conditions, activation of the anti-apoptotic molecule Akt was suppressed in the irradiated area, and levels of the pro-apoptotic protein BAX were increased. Intravitreal injection of a PI3K/Akt inhibitor immediately after PDT increased BAX levels and photoreceptor cell apoptosis. CONCLUSION: Cytotoxic stress caused by PDT, at levels that do not cause overt tissue damage, induces VEGF and activates Akt to rescue the neural tissue, suppressing BAX. Thus, the immediate and transient induction of VEGF after PDT is neuroprotective.

Transcriptional factors associated with epithelial-mesenchymal transition in choroidal neovascularization.

PURPOSE: To investigate the transcriptional factors associated with epithelial-mesenchymal transition (EMT) in choroidal neovascularization (CNV) secondary to age-related macular degeneration (AMD). METHODS: Paraffin sections of CNV obtained from patients with AMD (n = 12) were stained for transcriptional factors related to EMT, i.e., Snail, Slug, SIP1, and Twist. As a control, postmortem sections of ocular normal tissue were used. Furthermore, using a human retinal pigment epithelial (RPE) cell line (ARPE-19), reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence microscopy were performed to explore the cellular localization and expression levels of EMT-associated transcriptional factors upon cytokine stimulation. RESULTS: Of 12 specimens, 11 CNV tissues (91.6%) showed staining for Snail localized in cellular nuclei, particularly in those of RPE cells. Snail was strongly co-localized with α-smooth muscle antigen (SMA) in RPE cells. In contrast, postmortem human retina showed no Snail staining in RPE cells. Other transcriptional factors, Slug, Twist and SIP1 were not detected in CNV or normal human retina. In ARPE-19 cells, RT-PCR and immunofluorescence microscopy showed that Snail mRNA was upregulated by transforming growth factor (TGF)-ß and VEGF stimulation. Furthermore, TGF-ß induced relocalization of Snail to the nucleus in RPE cells. CONCLUSIONS: The current data indicate that Snail is a major transcriptional factor for EMT changes of RPE cells in human CNV.

Retinal ganglion cell loss in superoxide dismutase 1 deficiency.

PURPOSE: To investigate the influence of deficiency in superoxide dismutase (SOD) 1, a major antioxidative enzyme, on retinal ganglion cells (RGCs). METHODS: In the SOD1 total knockout (SOD1-deficient) mice, the level of superoxide anion was measured using dihydroethidium. The number of RGCs was counted in both the retinal sections and the flat-mount retinas after retrograde labeling. Thickness of nerve fiber layer (NFL) was measured in the sections, and the amount of neurofilament protein was measured by immunoblot analysis. Pattern electroretinogram (ERG), which reflects the function of retinal ganglion cells, dark-adapted ERG, and cone ERG were performed. The intraocular pressure (IOP) was measured with an induction-impact tonometer. The levels of SOD-1 and -2 were measured by ELISA, in the serum of 47 newly diagnosed consecutive normal tension glaucoma (NTG) patients and 44 consecutive control subjects. RESULTS: The level of superoxide anion in the RGC layer was significantly higher in 24-week-old SOD1-deficient mice than in wild-type mice. The RGC number was significantly reduced in 24-week-old SOD1-deficient mice, although they were not in 8-week-old mice. The NFL thickness and neurofilament protein were reduced in 24-week-old SOD1-deficient mice. The amplitude of pattern ERG was significantly reduced, although dark-adapted and cone ERGs showed no impairment, in 24-week-old SOD1-deficient mice. The IOP level was not changed in the SOD1-deficient mice. The serum level of SOD1, but not SOD2, was significantly lower in the NTG patients than in the healthy controls. CONCLUSIONS: SOD1 deficiency causes RGC vulnerability, which may be involved in the underlying condition of NTG.

Eicosapentaenoic acid suppresses ocular inflammation in endotoxin-induced uveitis.

PURPOSE: To investigate the effect of eicosapentaenoic acid (EPA) on acute ocular inflammation in an animal model of endotoxin-induced uveitis (EIU). METHODS: C57Bl/6 mice (6-week-old males) were orally treated with EPA at a dose of 50 mg/kg/day for 5 days. EIU was then induced in the animals by intraperitoneal injection of 160 microg lipopolysaccharide (LPS). Twenty-four hours after LPS injection, leukocyte adhesion to the retinal vasculature was evaluated by the concanavalin A lectin perfusion-labeling technique, and leukocyte infiltration into the vitreous cavity was quantified. Furthermore, the protein levels of monocyte chemotactic protein (MCP)-1, interleukin (IL)-6, intercellular adhesion molecule-1 and phospholyrated nuclear factor (NF)-kappaB p65 in the retina and retinal pigment epithelium (RPE)-choroid complex were examined by enzyme-linked immunosorbent assay (ELISA). RESULTS: At 24 h after LPS injection, the EIU animals treated with oral EPA administration showed a significant decrease in leukocyte adhesion to the retinal vessels by 43.4% (p<0.01) and leukocyte infiltration into the vitreous cavity by 49.2% (p<0.05). In addition, EPA significantly reduced the protein levels of MCP-1 and IL-6 in the retina and the RPE-choroid complex. Furthermore, phosphorylation of NF-kappaB was suppressed by EPA treatment. CONCLUSIONS: Our data suggest that EPA inhibits multiple inflammatory molecules in vivo. EPA may become a novel strategy in the prevention and/or treatment of ocular inflammatory diseases.

Retinal dysfunction and progressive retinal cell death in SOD1-deficient mice.

The superoxide dismutase (SOD) family is a major antioxidant system, and deficiency of Cu,Zn-superoxide dismutase (SOD1) in mice leads to many different phenotypes that resemble accelerated aging. The purpose of this study was to examine the morphology and physiology of the sensory retina in Sod1(-/-) mice. The amplitudes of the a- and b-waves of electroretinograms elicited by stimuli of different intensity were reduced in senescent Sod1(-/-) mice, and this reduction in amplitude was more pronounced with increasing age. Retinal morphometric analyses showed a reduced number of nuclei in both the inner nuclear cell layer and outer nuclear cell layer. Electron microscopy revealed swollen cells and degenerated mitochondria in the inner nuclear cell and outer nuclear cell layer of senescent Sod1(-/-) mice indicating necrotic cell death. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling revealed no significant differences in the number of apoptotic cells between Sod1(-/-) and wild-type mice, and activated caspase-3 could not be detected in the retina of Sod1(-/-) mice. In addition to the age-related macular degeneration-like phenotypes previously reported, Sod1(-/-) mice also present progressive retinal degeneration. Our results indicate that Sod1(-/-) mice may be a good model system in which to study the mechanism of reactive oxygen species-mediated retinal degeneration.