S. YARDIMCI1, S. ÇOMOĞLU2

1Ankara Üniversitesi Tıp Fakültesi, fizyoloji ABD
2Ankara Numune Hastanesi, Nöroloji Kliniği

Keywords: Diabetic polyneuropathy, oxidative damage, glycolisation end products, ischemia-reperfusion injury

Abstract

Obtained data have been pointed out that glycolisated biomolecules which accumulatein neurons become more sensitive to oxidation. It has been known that similarly with biomolecules found in cellulary compartments, glycolisated plasma lipoproteins oxidate easily according to the native forms of them. It has been revealed that oxidated forms of glycolisated plasma lipoproteins decrease the noronal blood flow by causing the microangiopathic changes in neurovascular bad by breaking the endotel-related relaxation function and activating of platelets in circulatory system. On the other hand, it has been understood that increase in oxygen consumption since glucose converts to sorbitol and fructose in activation of poliol pathway and decrease in noronal perfusion related to the microangiopathic changes in nörovascular system are enhanced the oxidative injury. According to these data, it has been accepted that oxidative damage in noronal tissue can be one of the most important metabolic changes mediates to the development of diabetic polyneuropathy.