Diabetic Cataract and Role of Antiglycating Phytochemicals

2019 ◽  
pp. 271-290 ◽  
Author(s):  
Vaishali Agte ◽  
Snehal Gite
Keyword(s):  
Diabetic Cataract

scholarly journals Lens Lipid Peroxides and Glutathione Concentrations in Diabetic Cataract

1997 ◽  
Vol 34 (2) ◽  
pp. 190-192 ◽  
Author(s):  
D Özmen ◽  
I Mutaf ◽  
B Özmen ◽  
J Mentes ◽  
O Bayindir
Keyword(s):  
G Protein ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Diabetic Cataract ◽  
Free Radical Damage ◽  
Significant Difference ◽  
Radical Damage

This study aims to explore the role of reactive oxygen radicals in the genesis of diabetic cataract. Lipid peroxide (LPO) concentrations in senile ( n = 30) and diabetic ( n = 14) cataractous lenses, were determined as thiobarbituric acid-reactive substances (TBARS) by a method modified from Satoh and Yagi, and reduced glutathione (GSH) concentrations were measured according to Beutler. Lens LPO levels (mean, SD; nmol TBARS/g protein) were significantly higher in diabetics (107·54, 18·12) than senile cataractous subjects (53·54, 15·48) ( P < 0·0001). Lens GSH levels (mean, SD; nmol/g protein) showed no significant difference between diabetics (4·29, 2·05) and senile cataractous subjects (4·68, 3·12). These results suggest that free radical damage is more effective in the genesis of diabetic cataract than in senile cataract.

Protective role of Borreria hispida against Galactosamine Induced Diabetic Cataract

2019 ◽  
Vol 12 (3) ◽  
pp. 1235
Author(s):  
M. Sumithra ◽  
Shatabdi Choudhury ◽  
L S Dhivya ◽  
M Nithiyanand ◽  
Jimson Zachariah ◽  
...  
Keyword(s):  
Protective Role ◽  
Diabetic Cataract

scholarly journals Diabetic cataract formation: potential role of glycosylation of lens crystallins.

1978 ◽  
Vol 75 (6) ◽  
pp. 2918-2922 ◽  
Author(s):  
V. J. Stevens ◽  
C. A. Rouzer ◽  
V. M. Monnier ◽  
A. Cerami
Keyword(s):  
Potential Role ◽  
Cataract Formation ◽  
Lens Crystallins ◽  
Diabetic Cataract ◽  
Formation Potential

scholarly journals microRNA-199a-5p regulates epithelial-to-mesenchymal transition in diabetic cataract by targeting SP1 gene

2020 ◽  
Vol 26 (1) ◽  
Author(s):  
Xin Liu ◽  
Qiaoyun Gong ◽  
Longfei Yang ◽  
Min Liu ◽  
Lingzhi Niu ◽  
...  
Keyword(s):  
Differential Expression ◽  
Epithelial To Mesenchymal Transition ◽  
Specific Protein ◽  
Luciferase Reporter ◽  
Diabetic Cataract ◽  
Mesenchymal Transition ◽  
Associated Proteins ◽  
Precise Role ◽  
Dual Luciferase Reporter Assay

Abstract Background As a common ocular complication of diabetes mellitus, diabetic cataract is becoming a leading cause of visual impairment. The progression of diabetic cataract progression involves epithelial-to-mesenchymal transition (EMT), the precise role of which remains to be investigated. As microRNAs (miRNAs) are suggested to be involved in the pathogenesis of many diseases, identification of aberrantly expressed miRNAs in diabetic lens epithelial cells (LECs) and their targets may provide insights into our understanding of diabetic cataract and potential therapeutic targets. Methods Diabetic cataract capsules and LECs exposed to high glucose (25 mmol/L, 1–5 days) were used to mimic the model. Quantitative RT-PCR was performed to evaluate the differential expression of miRNA. Dual luciferase reporter assay was used to identify the binding target of miR-199a-5p. The expression of EMT-associated proteins was determined by immunofluorescence and Western blot analysis. Results Our results showed the differential expression of miR-9, -16, -22, -199a and -204. MiR-199a was downregulated in diabetic cataract capsule and hyperglycemia-conditioned human LECs. Specific protein 1 could be directly targeted and regulated by miR-199a in LECs and inhibit EMT in diabetic LECs. Conclusion Our findings implied miR-199a could be a therapeutic target by regulating SP1 directly to affect EMT in diabetic cataract and provided novel insights into the pathogenesis of diabetic cataract.

scholarly journals Histone acetyltransferase and Polo-like kinase 3 inhibitors prevent rat galactose-induced cataract

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Fumito Kanada ◽  
Yoshihiro Takamura ◽  
Seiji Miyake ◽  
Kazuma Kamata ◽  
Mayumi Inami ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Histone Acetyltransferase ◽  
Ex Vivo ◽  
Causative Factor ◽  
Mrna Levels ◽  
Cataract Formation ◽  
Diabetic Cataract ◽  
Novel Approach ◽  
Hat Inhibitor

AbstractDiabetic cataracts can occur at an early age, causing visual impairment or blindness. The detailed molecular mechanisms of diabetic cataract formation remain incompletely understood, and there is no well-documented prophylactic agent. Galactose-fed rats and ex vivo treatment of lenses with galactose are used as models of diabetic cataract. To assess the role of histone acetyltransferases, we conducted cataract prevention screening with known histone acetyltransferase (HAT) inhibitors. Ex vivo treatment with a HAT inhibitor strongly inhibited the formation of lens turbidity in high-galactose conditions, while addition of a histone deacetylase (HDAC) inhibitor aggravated turbidity. We conducted a microarray to identify genes differentially regulated by HATs and HDACs, leading to discovery of a novel cataract causative factor, Plk3. Plk3 mRNA levels correlated with the degree of turbidity, and Plk3 inhibition alleviated galactose-induced cataract formation. These findings indicate that epigenetically controlled Plk3 influences cataract formation. Our results demonstrate a novel approach for prevention of diabetic cataract using HAT and Plk3 inhibitors.

scholarly journals Role of oxidative stress in cataractogenesis

2017 ◽  
Vol 5 (6) ◽  
pp. 2390 ◽  
Author(s):  
Geeta Bhatia ◽  
A. N. Sontakke ◽  
Subodhini Abhang
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Vitamin C ◽  
Protein Carbonyl ◽  
Diabetic Patients ◽  
Diabetic Cataract ◽  
Age Related ◽  
Antioxidant Defence System ◽  
Cataract Patients

Background: Cataract is a multifactorial disease and is a major cause of blindness in india. Oxidative stress is thought to be a major factor to initiate the process of cataractogenesis. It is today well established fact that oxidative stress participates in both age-related (senile) and diabetes-induced cataract (diabetic). Oxidative damage to the lens most likely arises as a consequence of an impaired antioxidant defence system, due to increased generation of ROS both by age and diabetes. The present study was designed to determine role of oxidative stress in cataractogensis and to compare levels of oxidative stress markers in senile and diabetic cataract patients.Methods: Serum malondialdehyde (MDA) and serum protein carbonyl (PC) were measured as indicator of oxidative stress whereas antioxidant status was assessed by estimating serum Total antioxidant capacity (TAC) and dietary antioxidants levels i.e vitamin C and vitamin E in senile and diabetic cataract patients compared with healthy controls.Results: The result reveal that the serum MDA and PC levels were significantly increased in patients with senile and diabetic cataract whereas serum TAC, vitamin C and Vitamin E were significantly reduced in senile and diabetic patients when compared with normal healthy controls.Conclusions: From the result, it is concluded that oxidative stress is in the foreground of cataract formation which includes senile and diabetic cataract. Oxidative stress produced in diabetic cataract patients is more as compared to senile cataract patients. 

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