Protective Effects of Inducible HO-1 on Oxygen Toxicity in Rat Brain Endothelial Microvessel Cells.
10.3803/EnM.2014.29.3.356
- Author:
Seung Jun YOO
1
;
Neal K NAKRA
;
Gabriele V RONNETT
;
Cheil MOON
Author Information
1. Department of Brain Science, Graduate School, Daegu Gyeungbuk Institute of Science and Technology (DGIST), Daegu, Korea. cmoon@dgist.ac.kr
- Publication Type:Original Article
- Keywords:
Heme;
Oxygenases;
Bilirubin;
Iron;
Carbon monoxide
- MeSH:
Animals;
Antioxidants;
Bilirubin;
Biliverdine;
Brain*;
Carbon Monoxide;
Cycloheximide;
DNA;
Guanosine Monophosphate;
Heme;
Heme Oxygenase (Decyclizing);
Hemin;
Iron;
Ischemia;
Lipid Peroxidation;
Microvessels*;
Oxidative Stress;
Oxygen*;
Oxygenases;
Rats*;
Reperfusion;
Reperfusion Injury;
Zinc
- From:Endocrinology and Metabolism
2014;29(3):356-362
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Reperfusion in ischemia is believed to generate cytotoxic oxidative stress, which mediates reperfusion injury. These stress conditions can initiate lipid peroxidation and damage to proteins, as well as promote DNA strand breaks. As biliverdin and bilirubin produced by heme oxygenase isoform 1 (HO-1) have antioxidant properties, the production of both antioxidants by HO-1 may help increase the resistance of the ischemic brain to oxidative stress. In the present study, the survival effect of HO-1 was confirmed using hemin. METHODS: To confirm the roles of HO-1, carbon monoxide, and cyclic guanosine monophosphate further in the antioxidant effect of HO-1 and bilirubin, cells were treated with cycloheximide, desferoxamine, and zinc deuteroporphyrin IX 2,4 bis glycol, respectively. RESULTS: HO-1 itself acted as an antioxidant. Furthermore, iron, rather than carbon monoxide, was involved in the HO-1-mediated survival effect. HO-1 activity was also important in providing bilirubin as an antioxidant. CONCLUSION: Our results suggested that HO-1 helped to increase the resistance of the ischemic brain to oxidative stress.
