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Purpose:Peak toxicity for in vivo ultraviolet radiation (UVR) exposure to the lens is in the 300-nm wavelength region. However, little is known about corneal cell damage at 300 nm. The purpose of the study was to determine the time evolution of apoptosis in the cornea after in vivo exposure to 300-nm UVR.Methods:Altogether, 16 Sprague Dawley rats were divided into 4 groups and unilaterally exposed to 5 kJ/m(2) UVR ((max): 300 nm; (0.5): 10 nm) for 15 minutes. After a predetermined latency period of 1, 5, 24, and 120 hours, depending on the group, the animals were killed and eyes were enucleated. Eye globes were further cryosectioned in 10-m thick midsagittal sections. For the detection of apoptosis, the TUNEL method was applied.Results:TUNEL-positive signals were observed in the superficial epithelial cells in the exposed and control eyes at all latency periods. At 5 hours, TUNEL staining was detected in the exposed corneas in epithelial cells, keratocytes, and endothelial cells with a maximum signal at 24 hours. At 120 hours, no TUNEL staining was found in endothelial cells and only occasionally in keratocytes in exposed corneas. Signs of ulceration and stromal thinning were observed at 120 hours.Conclusions:UVR in the 300-nm wavelength region induces TUNEL staining in all 3 corneal layers. TUNEL staining of all 3 corneal layers is an early postexposure event observed after a 5-hour latency period. Corneal sterile keratolysis occurs in the time window of 24 to 120 hours probably induced by neutrophils.

Introduction: Phacoemulsification is now commonly used surgical procedure for cataract. The endothelial celldamage duringphacoemulsification can be caused by factors such as irrigation flow, turbulence and movementof fluids, presence of air bubbles, direct trauma caused by the instruments or lens fragments, and the phacoemulsification time and power needed to achieve nuclear emulsification. Grade of nucleus sclerosis affect the corneal endothelial cell loss in phacoemulsification. Methods: We concluded the study in 500 cases of cataract and found that loss of corneal endothelial cells increases with increasing the grade of nucleus sclerosis. Many methods have evolved in recent years to enhance the efficacy of nuclear management during phacoemulsification. The main purpose of these techniques is to mechanically break the nucleus into smaller fragments with the help of a second instrument, which helps decrease the use of ultrasound power in nuclear emulsification and reduces surgical time and limiting endothelial damage. Results: The average percentage loss of cells during our study was 14.5% which was highly significant (0.981). Conclusion:In our study we concluded that the endothelial cell damage increases with increase in nucleus hardness.

Introduction: Phacoemulsification is now commonly used surgical procedure for cataract. The endothelial celldamage duringphacoemulsification can be caused by factors such as irrigation flow, turbulence and movementof fluids, presence of air bubbles, direct trauma caused by the instruments or lens fragments, and the phacoemulsification time and power needed to achieve nuclear emulsification. Grade of nucleus sclerosis affect the corneal endothelial cell loss in phacoemulsification. Methods: We concluded the study in 500 cases of cataract and found that loss of corneal endothelial cells increases with increasing the grade of nucleus sclerosis. Many methods have evolved in recent years to enhance the efficacy of nuclear management during phacoemulsification. The main purpose of these techniques is to mechanically break the nucleus into smaller fragments with the help of a second instrument, which helps decrease the use of ultrasound power in nuclear emulsification and reduces surgical time and limiting endothelial damage. Results: The average percentage loss of cells during our study was 14.5% which was highly significant (0.981). Conclusion:In our study we concluded that the endothelial cell damage increases with increase in nucleus hardness.