| dc.creator |
NAZIROĞLU, Mustafa |
|
| dc.date |
2010-12-31T22:00:00Z |
|
| dc.date.accessioned |
2020-10-06T09:27:19Z |
|
| dc.date.available |
2020-10-06T09:27:19Z |
|
| dc.identifier |
181633fb-c9f6-4960-8e72-6590ab88b14f |
|
| dc.identifier |
10.1007/978-1-61779-071-3_4 |
|
| dc.identifier |
https://avesis.sdu.edu.tr/publication/details/181633fb-c9f6-4960-8e72-6590ab88b14f/oai |
|
| dc.identifier.uri |
http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/54255 |
|
| dc.description |
Of all the organs in the body, the central nervous system is especially sensitive to free radical damage. Its high consumption of oxygen, rich content of easily oxidizable 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. Because 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 be responsible for activation of TRPM2 in neurological diseases. Genetic defects may have an important role in the etiology of bipolar diseases. Experimental studies with respect to patch-clamp and Ca2+ imaging, inhibitor roles of antioxidants are also summarized in the review. |
|
| dc.language |
eng |
|
| dc.rights |
info:eu-repo/semantics/closedAccess |
|
| dc.title |
TRPM2 Cation Channels and Oxidative Stress-Induced Neuronal Cell Death |
|
| dc.type |
info:eu-repo/semantics/article |
|