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Vucuttaki tum organlar ozellikle merkezi sinir sistemi, serbest radikal hasarina karsi duyarlidir. Beynin yuksek oksijen tuketimi, kolayca okside olabilen zengin yag asitlerini barindirmasi, diger organlara gore dusuk seviyede antioksidan enzim ve antioksidan icermesi onu serbest oksijen radikalleri tarafindan birincil hedef haline getirmektedir. Na+ ve Ca+2 iyonlarina gecirgen melastatine bagli “transient receptor potential 2 (TRPM2)” katyon kanallari ya Ca+2 ile uyum icinde olan ADP-riboz tarafindan ya da oksidatif stres (H2O2) tarafindan kanallarin enzimatik Nudix bolgesine bagladigi ve ADP-riboz pirofosfataz’in aktive oldugu rapor edilmistir. Bu enzim aktivasyonu sonucunda da TRPM2 kanallarinin acildigi gozlemlenmistir. Bu derleme calismasinda, noronal hucrelerde, TRPM2 inhibisyonuna yol actigi dusunulen ADPR ve H2O2 maddeleri tam anlasilmadigi icin norolojik hastaliklardaki bipolar hastaliklar kadar mikroglia, hipokampus ve beyindeki ADPR ve oksidatif stresin TRPM2 kanallari uzerindeki etkileri gozden gecirilmistir. Mikroglia ve hipokampal hucrelerde TRPM2 katyon kanallarinin hem ADPR hem de H2O2 tarafindan acildigi gozlemlendi. Buna ek olarak, norolojik hastaliklarda H2O2 nin TRPM2 aktivasyonundan sorumlu oldugu gozukuyor. Bipolar hastaliklarin etiyolojisinde genetik faktorler onemli rollere sahip olabilirler.    Of all the organs in the body, the central nervous system is especially sensitive to free radical damage. Its high consumption oxygen, rich content of easily oxidizible fatty acids, relatively low content of antioxidant enzymes and antioxidants, and the presence of high levels of iron make it a prime substrate for damage by ROS. The Na+ and Ca2+-permeable melastatin related transient receptor potential 2 (TRPM2) cation channels can be gated either by ADP-ribose (ADPR) in concert with Ca2+ or by hydrogen peroxide (H2O2), an experimental model for oxidative stress, binding to the channel’s enzymatic Nudix domain. Since the mechanisms that lead to TRPM2 inhibiting in response to ADPR and H2O2 are not understood in neuronal cells, we reviewed the effects of ADPR and oxidative stress in neurological cells such as microglia, hippocampus and brain as well as neurological diseases such as bipolar diseases. It was observed that TRPM2 cation channels in microglia and hippocampal cells were gated both by ADPR and H2O2. In addition, H2O2 seems to responsible activation of TRPM2 in neurological diseases. Genetic defects may be have important role in etiology of bipolar diseases.

Nörolojik Hücrelerde TRPM2 Katyon Kanallarının Moleküler Mekanizmalardaki Rolleri