Abstract
Abstract: :
Purpose: To verify the role of photo-oxidative stress in the induction of apoptosis after photorefractive keratectomy (PRK) excimer laser. Methods: Fourty male newzealand white rabbits (2.5 Kg) were used in this experiment,ten animals were served as controls. Thirty rabbits were subjected to PRK (96 mJ/cm2). 15 rabbits were scarified after 24 hours and the other15 were scarified after one month. Oxidative tissue damage after laser were determined by assaying the levels of reduced glutathione, malondialdehyde, nitric oxide and sFas levels in corneal and lens homogenate.Fractionation of soluble lens cortical proteins by column chromatography were also performed. Corneas and lenses were processed for transmission electron microscopy (TEM). Results Significantly lowered glutathione coupled to significantly higher malondialdehyde, nitric oxide and sFas levels in both corneal and lens homogenate were detected after 24 hours andone month PRK treatment compared to controls. TEM of corneas revealed the occurrance of apoptotic nuclei and cells after one month. TEM verfied the occurance of apoptosis in lens and showed breakdown of apoptotic cells by adjcent cells, no sign of necrosis. Conclusion:Keratocyte apoptosis is one of the main events after PRK leading to haze formation and regression of refraction. while, lens apoptosis may be a common cellular basis for intiation of oxidative cataractogenesis after PRK.
Keywords: apoptosis/cell death • oxidation/oxidative or free radical damage • refractive surgery: complications