Spatial targeted delivery of riboflavin with a controlled corneal iontophoresis delivery system in theranostic-guided UV-A light photo-therapy.

Seven human donor eye globes underwent corneal cross-linking using theranostic UV-A device with accessory corneal iontophoresis system for patterned delivery of a 0.22% riboflavin solution. Theranostic-guided UV-A light illumination assessed riboflavin distribution and treated corneas at 10 mW/cm2 for 9 min with a 5.0-mm beam size. Corneal topography maps were taken at baseline and 2-h post-treatment. Analysis utilized corneal topography elevation data, with results showing controlled riboflavin delivery led to a consistent gradient, with 40% higher levels centrally (248 ± 79 µg/cm3) than peripherally (180 ± 72 µg/cm3 at ±2.5 mm from the center). Theranostic-guided UV-A light irradiation resulted in significant changes in corneal topography, with a decrease in best-fit sphere value (-0.7 ± 0.2 D; p < 0.001) and consistent downward shift in corneal elevation map (-11.7 ± 3.7 µm). The coefficient of variation was 2.5%, indicating high procedure performance in achieving significant and reliable corneal flattening.

Evidence for persistent UV-induced DNA damage and altered DNA damage response in xeroderma pigmentosa patient corneas.

Xeroderma pigmentosum (XP) is a rare genetic disorder characterized by injury to the ocular surface due to exposure to ultraviolet (UV) radiation. UV-induced damage in the cells leads to the formation of cyclobutane pyrimidine dimers (CPDs) and 6-4 pyrimidine-pyrimidone photoproducts that are repaired by the NER (Nucleotide Excision Repair) pathway. Mutations in the genes coding for NER proteins, as reported in XP patients, would lead to sub-optimal damage repair resulting in clinical signs varying from photo-keratitis to cancerous lesions on the ocular surface. Here, we aimed to provide evidence for the accumulation of DNA damage and activation of DNA repair pathway proteins in the corneal cells of patients with XP. Corneal buttons of patients who underwent penetrating keratoplasty were stained to quantify DNA damage and the presence of activated DNA damage response proteins (DDR) using specific antibodies. Positive staining for pH2A.X and thymidine dimers confirmed the presence of DNA damage in the corneal cells. Positive cells were found in both control corneas and XP samples however, unlike normal tissues, positive cells were found in all cell layers of XP samples indicating that these cells were sensitive to very low levels of UV. pH2A.X-positive cells were significantly more in XP corneas (p < 0.05) indicating the presence of double strand breaks in these tissues. A positive expression of phosphorylated-forms of DDR proteins was noted in XP corneas (unlike controls) such as ataxia telangiectasia mutated/Rad-3 related proteins (ATM/ATR), breast cancer-1 and checkpoint kinases-1 and -2. Nuclear localization of XPA was noted in XP samples which co-localized (calculated using Pearson's correlation) with pATM (0.9 ± 0.007) and pATR (0.6 ± 0.053). The increased presence of these in the nucleus confirms that unresolved DNA damage was accumulating in these cells thereby leading to prolonged activation of the damage response proteins. An increase in pp53 and TUNEL positive cells in the XP corneas indicated cell death likely driven by the p53 pathway. For comparison, cultured normal corneal epithelial cells were exposed to UV-radiation and stained for DDR proteins at 3, 6 and 24 h after irradiation to quantify the time taken by cells with intact DDR pathway to repair damage. These cells, when exposed to UV showed nuclear translocation of DDR proteins at 3 and 6 h which reduced significantly by 24 h confirming that the damaged DNA was being actively repaired leading to cell survival. The persistent presence of the DDR proteins in XP corneas indicates that damage is being actively recognized and DNA replication is stalled, thereby causing accumulation of damaged DNA leading to cell death, which would explain the cancer incidence and cell loss reported in these patients.

Ocular surface changes in patients who have undergone head and neck radiation therapy.

PURPOSE: Dry eye syndrome (DES) is a familiar sequelae of radiation therapy (RT) for head and neck cancers (HNC). Ocular surface changes such as DES occur due to injury to the conjunctival epithelium, goblet cells, corneal surface, lacrimal glands, and meibomian glands. This study aimed at the evaluation and early detection of changes in ocular surface parameters in patients receiving RT for extraocular HNC. METHODS: Forty-two eyes of 21 patients undergoing HNC RT were evaluated. Radiation technique and dose of radiation to the lens and eye were recorded. Subjects were evaluated for meibomian gland changes by meiboscore grading, ocular surface disease index (OSDI) questionnaire, Schirmer's test, tear film break-up time (TBUT), and slit-lamp examination before RT, immediately post RT, and 6 weeks post RT. A comparison of the ipsilateral eye on the irradiated side to the contralateral eye was done. RESULTS: A significant reduction in TBUT was seen immediately post RT and 6 weeks post RT ( P < 0.001 and 0.008, respectively), with an increase in meiboscore at both visits ( P < 0.001). An OSDI score of >13 was seen in 23.80% of patients post RT, with a significant difference from baseline ( P < 0.001). On comparing ipsilateral and contralateral eye groups, a significant difference from baseline was seen in TBUT ( P < 0.001 and 0.033, respectively) and meiboscore ( P < 0.001 for both eyes). A significant change of >1 second in TBUT and >1.7 in meiboscore was seen with a mean dose of around 8 Gy to the lens. CONCLUSION: All patients undergoing HNC RT should be followed up for ocular surface and meibomian gland changes. The contralateral eye should also be evaluated. Patients receiving lower doses to the ocular structures should also be kept under follow-up.

Effect of light intensity on the tear production, central corneal thickness, and intraocular pressure in broiler chickens.

OBJECTIVE: The objective of the present study was to examine the effect of different light intensities on tear production, corneal thickness, and intraocular pressure in broilers. ANIMALS STUDIED: Both eyes of 72 male broilers were evaluated in this study. MATERIALS AND METHODS: Broilers were divided into the following three groups: low light intensity (n = 24, 5 lux), moderate light intensity (n = 24, 20 lux), and high light intensity (n = 24, 80 lux). The eyes of all birds (n = 72) underwent a complete ophthalmic examination, which included the Schirmer tear test (STT-I), intraocular pressure (IOP), and the central cornea thickness measurement (CCT). The effect of light intensity on the Schirmer test, intraocular pressure, and central corneal thickness values was examined at eye and animal level (right and left eyes separately and cumulatively/no distinguishing left or right) by using one-way ANOVA. RESULTS: At the animal level, without discrimination of left and right eye measurements, statistically significant differences were found between 5-20 and 20-80 lux groups on IOP measurements (p < .05). The difference in CCT measurements between the 5 and 20 lux groups was statistically significant (p < .05), and the corneal thickness of the 5 lux group animals was found to be statistically significant and higher than the 20 lux group (p < .05). CONCLUSIONS: In conclusion, light intensity has an influence on eye health in broilers. Present results may attribute to the future studies as a reference value for broilers raised under different light intensities.

Alleviation of the Genotoxic Effect of Experimental Circulatory Brain Hypoxia in Rat Cornea under the Effect of Infrared Low-Level Laser Radiation.

Experimental modeling of oxidative stress was conducted by creating circulatory brain hypoxia, accompanied by development of free radical processes leading to genome instability through an example of anterior epithelial layer of rat cornea. We studied the influence of infrared low-level laser radiation (ILLLR) in the therapeutic dose and mode (pulse power 8 W, λ=0.89 µm). Exposure of animals with circulatory brain hypoxia (ischemia) to ILLLR reduced the level of chromosome aberrations in corneal epitheliocytes and led to change in the mitotic index. Correction of the damaging effects of ischemia in the experiment in the absence of mutagenic effect of ILLLR in therapeutic dose and mode of exposure indicates the possibility of applying this physical method for correcting after-effects of oxidative stress during progression of degenerative eye diseases in ophthalmic practice.

Effects of water-filtered infrared A and visible light (wIRA/VIS) radiation on heat- and stress-responsive proteins in the retina and cornea of guinea pigs.

Water-filtered infrared A and visible light (wIRA/VIS), shown to reduce chlamydial infections in vitro and in vivo, might represent an innovative therapeutic approach against trachoma, a neglected tropical disease caused by ocular infection with the bacterium C. trachomatis. In this in vivo study, we assessed the impact of wIRA radiation in combination with VIS (wavelength range 595-1400 nm, intensity 2100 W/m2) on the retina and cornea in a guinea pig animal model of inclusion conjunctivitis. We investigated the effects 19 days after wIRA/VIS irradiation by comparing a single and double wIRA/VIS treatment with a sham control. By immunolabeling and western blot analyses of critical heat- and stress-responsive proteins, we could not detect wIRA/VIS-induced changes in their expression pattern. Also, immunolabeling of specific retinal marker proteins revealed no changes in their expression pattern caused by the treatment. Our preclinical study suggests wIRA/VIS as a promising and safe therapeutic tool to treat ocular chlamydial infections.

Experimental in-vitro investigation on Epi-Off-Crosslinking on porcine corneas.

AIM: To evaluate quantitatively the effects of the Epi-Off-CXL irradiance dose on the stromal stiffening of pig corneas. SETTING: Laboratory of Biological structures (LaBS), Politecnico di Milano, Milano, Italy. METHODS: Inflation tests have been carried on 90 excised and de-epithelized pig corneas, monitoring the change of configuration of the corneal dome at specific pressures. Test have been carried out twice on each cornea, once before and once after Epi-Off-CXL performed at a constant irradiance of 9 mW/cm2 and variable UV-A exposure times. Corneas were grouped according to the exposure time (2.5, 5, 10, 15 and 20 min), proportional to the irradiation dose (1.35, 2.7, 5.4, 8.1, and 10.8 J/cm2). A theoretical model based on linearized shell theory has been used to estimate the increment of the corneal stiffness. RESULTS: The linearized shell theory allowed to establish a quantitative relation between the increment of the stiffness parameters and the irradiation dose. Relative to the pre-treatment values, in all experiments the post-treatment corneal stiffness revealed a pronounced increase. In general, the stiffness gain increased with the exposure time. No significant differences in stiffening was observed between tests conducted at 2.5, 5, and 10 min exposure. CONCLUSIONS: Qualitatively, the effectiveness of accelerated CXL treatments observed in pig corneas complies very well with in-vivo clinical results in humans, suggesting that experimental data in pigs can be very useful for the design of the procedure in humans. A larger irradiation dose provides a larger increment of the corneal stiffness. Due to the biological variability of the tissues, however, it is difficult to distinguish quantitatively the level of the reinforcement induced by accelerated protocols (low doses with < = 10 min exposure), less prone to induce damage in the corneal tissue. Therefore, the definition of personalized treatments must be related to the actual biomechanics of the cornea.

The T414G mitochondrial DNA mutation: a biomarker of ageing in human eye.

The mitochondrial mutation T414G (mtDNAT414G) has been shown to accumulate in aged and sun-exposed skin. The human eye is also exposed to solar harmful rays. More precisely, the anterior structures of the eye (cornea, iris) filter UV rays and the posterior portion of the eye (retina) is exposed to visible light. These rays can catalyse mutations in mitochondrial DNA such as the mtDNAT414G, but the latter has never been investigated in the human ocular structures. In this study, we have developed a technique to precisely assess the occurrence of mtDNAT414G. Using this technique, we have quantified mtDNAT414G in different human ocular structures. We found an age-dependent accumulation of mtDNAT414G in the corneal stroma, the cellular layer conferring transparency and rigidity to the human cornea, and in the iris. Since cornea and iris are two anterior ocular structures exposed to solar UV rays, this suggests that the mtDNAT414G mutation is resulting from cumulative solar exposure and this could make the mtDNAT414G a good marker of solar exposure. We have previously shown that the mtDNACD4977 and mtDNA3895 deletions accumulate over time in photo-exposed ocular structures. With the addition of mtDNAT414G mutation, it becomes feasible to combine the levels of these different mtDNA mutations to obtain an accurate assessment of the solar exposure that an individual has accumulated during his/her lifetime.

UV-Photokeratitis Associated with Germicidal Lamps Purchased during the COVID-19 Pandemic.

PURPOSE: To report photokeratitis caused by the improper use of germicidal lamps purchased during the COVID-19 pandemic. METHODS: Case series. RESULTS: Seven patients presented with acute ocular surface pain after exposure to UV-emitting germicidal lamps. Visual acuity was 20/30 or better in 13 of 14 eyes (93%). Anterior segment examination revealed varying degrees of conjunctival injection and diffusely distributed punctate epithelial erosions (PEEs) in every patient. No intraocular inflammation was identified across the cohort and all fundus examinations were normal. Treatment varied by provider and included artificial tears alone or in combination with antibiotic ointments and/or topical steroids. Five patients were followed via telehealth, one patient returned for an in-office visit, and one patient was lost to follow-up. Five of six patients endorsed complete resolution of symptoms within 2-3 days. CONCLUSIONS: Patients should follow manufacturer recommendations when using UV-emitting germicidal lamps and avoid direct exposure to the ocular surface.

Effects on the Ocular Surface from Reading on Different Smartphone Screens: A Prospective Randomized Controlled Study.

The purpose of this study was to investigate the influence of smartphone reading on the ocular surface and to compare the various effects of different screens and light conditions on the ocular surface. One hundred nineteen volunteers were randomly divided into: light + organic light-emitting diode (OLED), light + electronic ink (eINK), dark + OLED, and dark + eINK. Ocular surface examinations, including noninvasive break-up time (NIBUT), noninvasive keratograph tear meniscus height (NIKTMH), ocular redness, fluorescein break-up time (FBUT), corneal fluorescein staining, meibomian gland assessment, Schirmer I Test, and blinking frequency, were performed before and after a reading task. Symptoms were evaluated using the Ocular Surface Disease Index (OSDI) and Computer Vision Syndrome Questionnaire (CVS-Q). NIBUT and FBUT were decreased statistically significantly after participants read on an OLED screen for 2 hours compared with the baseline in light and dark environments, whereas no statistically significant decrease was observed on an eINK screen. NIKTMH was statistically significantly decreased after reading on an OLED screen in light and dark settings, and the eINK screen had a lesser effect on NIKTMH. An obvious increase in the ocular redness, OSDI and CVS-Q scores was observed after reading on an OLED screen, whereas the eINK screen had a lesser effect on these indicators. Blink rate increased gradually in OLED subgroups during the reading task, whereas no statistically significant difference was observed in the eINK subgroups. Our research suggested that reading on an OLED screen can cause ocular surface disorder and obvious subjective discomfort, whereas reading on an eINK screen can minimize ocular surface disorder in both dark and light environments.

Revisiting 35 and 94 GHZ Millimeter Wave Exposure to the Non-Human Primate Eye.

A previous study reported thermal effects resulting from millimeter wave exposures at 35 and 94 GHz on non-human primates, specifically rhesus monkeys' (Macaca mulatta) corneas, but the data exhibited large variations in the observed temperatures and uncertainties in the millimeter wave dosimetry. By incorporating improvements in models and dosimetry, a non-human primate experiment was conducted involving corneal exposures that agreed well with a three-layer, one-dimensional, thermodynamic model to predict the expected surface temperature rise. The new data indicated that the originally reported safety margins for eye exposures were underestimated by 41 ± 20% over the power densities explored. As a result, the expected minimal visible lesion thresholds should be raised to 10.6 ± 1.5 and 7.1 ± 1.0 J cm at 35 and 94 GHz, respectively, provided that the power density is less than 6 W cm for subjects that are unable to blink. If the blink reflex was active, a power density threshold of 20 W cm could be used to protect the eye, although the eyelid could be burned if the exposure was long enough.

The microanatomy of Bowman's layer in the cornea of the pig: Changes in collagen fibril architecture at the corneoscleral limbus

In most animals, Bowman's layer is a feature of the cornea of the eye, and lies between the sur-face epithelium and the stromal extracellular matrix that makes up the bulk of the cornea. It is comprised of a condensation of disorganised collagen fibrils. However, it has been conjectured that not all species possess Bowman’s layer, and pigs are a species that has classically been stated to lack this anatomical structure, although there is disagreement in the published literature. Here, we studied the porcine cornea using transmission and scanning electron microscopy (TEM and SEM) to ascertain whether Bowman’s layer existed. TEM identified a thin band of disorganised collagen fibrils between the epithelial basement membrane and corneal stroma. SEM images of the central and peripheral corneal surfaces, following removal of the corneal epithelium by cell maceration, revealed a disorganised meshwork of collagen fibrils, with a highly aligned annulus of collagen at the limbus. In between the peripheral cornea and limbus, a "transition zone" is observed where collagenfibrils start to align. Quantification of fibril alignment demonstrates a significant increase in collagen alignment from 0.08 ± 0.04 to 0.33 ± 0.07 (p < 0.001; n = 60; 0 = no alignment, 1 = full alignment) with increasing distance from the corneal centre. These data together lead us to conclude that the porcine cornea does include Bowman's layer, though it is thin (contributing roughly 0.2% of corneal thickness), and thus, reaffirms the porcine cornea's similarity to its human counterpart and usefulness as a model system

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Comparison of ophthalmic toxicity of light-emitting diode and organic light-emitting diode light sources.

The use of organic light-emitting diodes (OLEDs) has rapidly increased in recent years. However, the effect of OLEDs on human health has not been studied yet. We investigated morphologic and functional changes after OLEDs exposure of human ocular cells, including corneal, conjunctival, lens, and retinal pigment epithelial cells, and mouse eyes. In corneal and conjunctival epithelial cells, the levels of reactive oxygen species production and interleukin-8 expression after white light-emitting diodes (LED) exposure were significantly greater than those after OLED exposure. Although no gross morphologic changes of the eyelid or cornea were found in LED- or OLED-exposed mice, oxidative stress on ocular surface was significantly increased, and the outer nuclear layer (ONL) was significantly shorter in both light-treated groups than the control group. Moreover, ONL thickness was significantly lower in the LED group than the OLED group. The electroretinography response was significantly lower in light exposure group, and there was significant difference between LED- and OLED-treated mice. Although OLED exhibits certain ocular toxicity, it can be less toxic to eyes than LED. The higher blue-wavelength energy of LED light might be the reason for its higher toxicity relative to OLED.

MiR-205-3p protects human corneal epithelial cells from ultraviolet damage by inhibiting autophagy via targeting TLR4/NF-κB signaling.

OBJECTIVE: MiRNA has been found to have therapeutic effect on corneal damage. This paper aimed to study the effect of miR-205-3p on corneal damage induced by ultraviolet (UV) radiation. MATERIALS AND METHODS: HCE cells were exposed to UV light and transfected. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot were used to determine miRNA/mRNA and protein expression. CCK-8 assay, Edu incorporation experiment, and flow cytometry were used to separately measure cell activity, proliferation and apoptosis. LC3 puncta were researched by immunofluorescence experiment. TNF-α, IL-6 and IL-1ß levels in cells were detected by enzyme-linked immunosorbent assay (ELISA) kit. MDA, SOD, and GSH-PX levels were measured using detection kits. Reactive oxygen species (ROS) level was reflected by detecting DCFH-DA density. Luciferase activity assay was performed to verify the regulating relationship between miR-205-3p and TLR4. RESULTS: UV radiation decreased HCE cell viability, proliferation, and increased HCE cell apoptosis and autophagy (all p < 0.01). When exposed UV radiation, the overexpression of miR-205-3p group elevated HCE cells viability, proliferation and weakened HCE cells apoptosis and autophagy (all p < 0.01). MiR-205-3p inhibited inflammation and oxidative stress in HCE cells induced by UV radiation (p < 0.01). MiR-205-3p directly inhibited TLR4 expression. The upregulation of TLR4 significantly reversed the effects of miR-205-3p on HCE cells phenotypes induced by UV radiation (p < 0.01). CONCLUSIONS: MiR-205-3p protected HCE cells from UV damage by inhibiting autophagy via targeting TLR4.

Protective Effect of Vitamin C against Infancy Rat Corneal Injury Caused by Acute UVB Irradiation.

PURPOSE: Studies have shown that corneas of young children were more susceptible to Ultraviolet B (UVB) radiation damage. However, there exist limited information about the harm of UVB to eyes and preventive measures on infancy. Vitamin C as an antioxidant is widely used to prevent many diseases. Therefore, the aim of this study was to explore the protective effect of vitamin C on the cornea of infant rats with acute UVB injury. METHOD: Thirty-six infant rats were randomly divided into three groups: control (CON) group, UVB (UVB) group, and UVB+vitamin C (UVB+VitC) group. The UVB group was exposed to UVB irradiation (8 J/cm2, 15 min/d, 7 d) and the UVB+vitamin C group suffered the same UVB irradiation treated with vitamin C at the dose of 40 mg/kg via intraperitoneal injection. Then, corneal morphology was detected in vivo and in vitro at 7 d post-UVB exposure. Furthermore, serum inflammatory factors (IL-1, IL-6, and TNF-α) and oxidative status (4-HNE and MDA) were detected by ELISA, and the expression of vascular endothelial growth factor-α (VEGF-α) and superoxide dismutase (SOD) in the cornea was detected by western blot or immunofluorescent staining. RESULTS: Slit lamp detection revealed that the area of corneal desquamation and corneal neovascularization in the UVB+VitC group was significantly less than those in the UVB group at 7 d post-UVB exposure (all p < 0.05). OCT results showed that the thickness of the central cornea in the UVB+VitC group was decreased than that in the UVB group (p < 0.05). The serum inflammatory factors (IL-1, IL-6, and TNF-α) and oxidative status (4-HNE and MDA) in the UVB group were significantly increased compared with the CON group (all p < 0.05), while those factors in the UVB+VitC group were decreased compared with those in the UVB group. Furthermore, the expression of VEGF-α in the UVB+VitC group was dramatically decreased compared with that in the UVB group (p < 0.05), and the expression of SOD2 in the UVB+VitC group was dramatically increased compared with that in the UVB group at 7 d post-UVB exposure (p < 0.05). CONCLUSION: Vitamin C could protect infant rats from corneal injury induced by UVB via alleviating corneal edema, improving corneal inflammatory reaction, and decreasing VEGF-α expression.

Corneal Damage Effects Induced by a 770-2,500 nm Supercontinuum Light Source.

BACKGROUND AND OBJECTIVES: Widespread applications of supercontinuum (SC) source lead to the possibility of ocular damages. However, the corneal damage effects induced by SC have not been explored before. The objectives of this study are to determine the rabbit corneal injury threshold for SC radiation and to examine whether the existing safety guidelines and standards are suitable for the hazard evaluation of this new kind of light source. STUDY DESIGN/MATERIALS AND METHODS: A series of experiments was conducted in the New Zealand white rabbit model to determine the corneal damage thresholds induced by a 770-2,500 nm SC source, with a corneal 1/e beam diameter of 0.37 mm. Through slit-lamp biomicroscope, optical coherence tomography (OCT), and histopathology the corneal damage characteristics at the threshold level were revealed. By employing the action spectra determined through the analysis of safety guidelines and standards, the damage thresholds for SC source could be compared with the corresponding exposure limits. RESULTS: The determined damage thresholds given in terms of the peak radiant exposure for exposure durations of 2.0 and 10.0 seconds were 2.1 × 103 and 7.4 × 103 J/cm2 , respectively. At threshold level, corneal damages involved the epithelium and the shallower stroma, and no obvious changes could be found in the deep stroma, Descemet's membrane, and endothelium. CONCLUSIONS: The exposure limits for the anterior parts of the eye in the wavelength range of 700-1,200 nm are overly conservative. The obtained results contribute to the knowledge base for the hazard evaluation of SC source. Lasers Surg. Med. © 2019 Wiley Periodicals, Inc.

Strong bonding of corneal incisions using a noncontact fiber-optic laser soldering method.

Suturing of corneal incisions requires significant skill. We demonstrate a noncontact method that will simplify the bonding process. 5-mm-long penetrating vertical and slanted incisions were made in corneas of eyes, extracted from dead piglets. A fiber-optic laser system was used for laser soldering of the incisions, under close temperature control, using albumin solder. The burst-pressure PB immediately after the soldering was found to be PB ≈ 92 and 875 mmHg, for vertical and slanted incisions, respectively. PB = 875 mmHg is an exceptionally high figure, ≈10 times the clinically acceptable value for sutured incisions. Laser soldering was then performed on penetrating incisions made in the corneas of live healthy piglets, of weight ≈10 Kg. After a healing period, the eyes were extracted, and the corneas were examined by histopathology and by optical coherence tomography. Our method immediately generated watertight and strong bonding without noticeable corneal shape distortion. These results would be beneficial for cataract surgery and for corneal transplantations. The fiber-optic system makes it much easier to bond corneal incisions. In the future, laser soldering could be automated and efficiently used by less experienced surgeons, thereby reducing the workload on the experienced ones.

The Healing of Oxidative Injuries with Trehalose in UVB-Irradiated Rabbit Corneas.

Our previous research revealed that trehalose, a nonreducing disaccharide of glucose and an important stress responsive factor, proved to have anti-inflammatory, antiapoptotic, and particularly antioxidant properties in UVB-irradiated corneas. Trehalose reduced oxidative stress in corneas induced by UVB irradiation, by means of a decrease in the antioxidant/prooxidant imbalance in the corneal epithelium. In this study, we demonstrate that trehalose of 3% or 6% concentration in eye drops directly decreases oxidative stress in UVB-irradiated corneas, by removing the excessive amount of reactive oxygen species (ROS). Trehalose drops applied on corneas during UVB irradiation once daily for four days resulted in a reduction or even absence of the oxidative stress, DNA damage, and peroxynitrite formation (detected by nitrotyrosine residues), seen in buffer-treated corneas. Furthermore, trehalose treatment applied curatively after repeated irradiation for the subsequent fourteen days led to the renewal of corneal transparency and significant suppression or even absence of neovascularization. This was in contrast to buffer-treated irradiated corneas, where the intracorneal inflammation was developed and the untransparent corneas were vascularized. In conclusion, the treatment of UVB-irradiated corneas with trehalose eye drops removed the excessive amount of ROS in the corneal epithelium, leading to the suppression of oxidative stress and favorable corneal healing. The 6% trehalose showed a higher intensive antioxidant effect.