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Abstract Cataract (or opacity of the crystalline lens) is one of the major causes of impaired vision and blindness worldwide affecting more than 17 million people around the world. Cataractogenesis is one of the often seen consequences of aging process, and diabetes mellitus is a major risk factor for the development of cataract at an early age compared to senile cataract. Advanced glycation end products (AGEs) are heterogeneous fluorescent derivatives formed by the Maillard process, a non-enzymatic reaction between the reducing sugars and the free amino groups of proteins, lipids and nucleic acids. AGEs play a pivotal role in cataractogenesis. Production of AGEs takes place throughout the normal aging process but its accumulation is found to be accelerated in diabetes. Advanced glycation end products formation and cataract progression are extremely slow processes and are triggered in the presence of free radicals. Oxidative stress along with AGEs may integrate resulting in acceleration of cataract formation. Obesity has also been proposed to be a risk factor for cataract development. Obesity has been linked to cataract by its associated complications such as diabetes. The purposes of this study are to investigate the potential role of advanced glycation end products (AGEs) in age-related (senile) and diabetic cataract subjects. In addition, this study is designed to determine the possible role of obesity in the development and progression of diabetic cataract. This study was conducted according to the Ethical Committee Approval of the Research Institute of Ophthalmology, Egypt on 40 patients, 20 of them were senile cataract patients. The other 20 patients were diabetic cataract, in addition to 20 subjects served as control group. The body mass index (BMI) was measured and the levels of FBG, HbA1c, MDA, TAC, GSH, SOD, and AGEs were determined in all subjects. Also, a comparative experimental study was performed on 40 rats for the detection of the modification of lens crystallin with glycation and obesity. The animals were divided into four groups of 10 animals each: control (group I); diabetic (group II) injected with a dose of 40 mg/kg by streptozotosin, high fat diet (Group III) were access to high fat diet and (Group IV) were access to a high fat diet and injected individually with a dose of 40 mg/kg by streptozotosin. There was no significant change in the body mass index (BMI) among the groups. There were significant increases in FBG and HbA1c in the diabetic cataract group compared to senile cataract and control groups. However, there was statistical significant increase in plasma MDA and AGEs levels in both the senile and diabetic cataract groups compared to control group. On the other hand, there were significant decreases in TAC, GSH, SOD activities in both the senile and diabetic cataract groups compared to control group. In the experimental study, there was a statistical significant increase in FBG, HbA1c, MDA and AGEs levels in diabetic and HFD groups compared to control group. However, there were statistical significant decreases in GSH and SOD activities in diabetic and HFD groups compared to control group. On the other hand, there were statistical significant decreases in TAC level and total lens protein in diabetic groups compared to control group but no significant decrease in 123 Summary and Conclusion TAC level and total lens protein in HFD group compared to control group. Sodium dodecyl sulfate (SDS) electrophoresis showed aggregation of lens proteins in the diabetic groups compared to HFD and control groups. This aggregation of lens proteins is an indicator of accelerated cataractogenesis. In conclusion, this study clearly demonstrated increased accumulation of AGEs, and increased lipid peroxidation products along with impaired antioxidant status in patients with both diabetic and senile cataract. Proper control of hyperglycemia, blocking of AGEs pathways by AGEs-inhibitors and low fat diet may be beneficial to delay cataract development. |