Katarak Diabetes

Arti Lukitasari

Abstract


Abstrak. Sebagian besar  (78%) pemecahan glukosa didalam lensa melalui jalur glikolisis anaerobik, 14% melalui jalur pentosa fosfat, sekitar 5% melalui jalur poliol. Pada kondisi hiperglikemia, jalur glikolisis anaerobik cepat jenuh,  dan glukosa akan memilih jalur poliol.   Pada jalur poliol glukosa dirubah menjadi sorbitol. Pada keadaan dimana sorbitol dipecah menjadi fruktosa oleh enzym Polyol Dehydrogenase,  namun pada Diabetes Mellitus kadar enzym Polyol Dehydrogenase rendah sehingga sorbitol menumpuk di dalam lensa mata.  Keadaan kondisi hipertonik  akan menarik masuk cairan akuos ke dalam lensa mata, merusak arsitektur lensa dan terjadi kekeruhan lensa.

Abstrack. Most of glucose solution (78%)  in the lens through anaerobic glycolysis, 14% through the pentose phosphate, about 5% through the polyol. In conditions of hyperglycemia, saturated fast lane anaerobic glycolysis, and glucose will choose the path of polyol. In the polyol path altered glucose to sorbitol. In circumstances where sorbitol is broken down into fructose by polyol dehydrogenase enzymes, but in Diabetes Mellitus polyol dehydrogenase enzyme levels low so that sorbitol accumulates in the lens of the eye.Hypertonic condition of the aqueous liquid will attract entry into the lens of the eye, damaging the lens of architecture and place the lens opacities.


Keywords


katarak; diabetik katarack; diabetic

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References


Jaffe NS, Horwitz J. Lens and Cataract. In : (Podos SM, Yanoff M, eds) Textbook of Ophthalmology. Gower Medical Publishing, New York.1992. 1:1 – 8

Gondhowiardjo TD. Aktivitas Enzim Aldehid Dehidrogenase pada Lensa Katarak Diabetes dan Non Diabetes. Ophthalmologica Indonesiana. 1996. 16 (2) : 118 – 124

Richard S, Tamas C, Sell DR, Monnier VM. Tissue-specific effects of aldose reductase inhibition on fluorescence and cross-linking of extracellular matrix in chronic galactosemia. Relationship to pentosidine cross-links. Diabetes 1991.40 (8) : 1049 – 1056.

Lee AYW, Chung SSM. Contribution of polyol pathway to oxidative stress in diabetic cataract. The FASEB Journal 1999. 13 : 23 – 30

Lewis S, Karrer J, Saleh S, et al,. Synthesis and evaluation of novel aldose reductase inhibitors: effect on lens protein kinase C. Molecular Vision 2001. 7: 164 - 71.

Halliwell B, Gutteridge JMC. Oxygen is a toxic gas, an introduction to oxygen toxicity and reactive oxygen species. In : Free Radicals in Biology and Medicine. 3rd edition. Oxford University Press New York.1999: 1 - 350.

Suryohudoyo P. Oksigen, anti oksidan dan radikal bebas. Kapita Selecta Ilmu Kedokteran Molekular. Edisi 1. Informedika, Jakarta. 2000: 31 - 47

Gillery P, Monboisse JC, Maquart FX, Borel JP. Aging Mechanisms of Proteins. Diabetes Metab. 1991. 17 (1) : 1 – 16.

Yan H, Harding JJ. Glycation induced inactivation and loss of antigenicity of catalase and superoxide dismutase. Biochem J 1997.328 : 599 – 605

Alan WS,. Advanced glycation : an important pathological event in diabetic and age related ocular disease. Br J Ophthalmol 2000. 85 : 746 – 753

Turk Z, Misur I, Turk N. Temporal Association between Lens Protein Glycation and Cataract Development in Diabetic Rats. Acta Diabetol. 1997.34 (1) : 49 – 54


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