TY - JOUR
T1 - Protective effects of inducible HO-1 on oxygen toxicity in rat brain endothelial microvessel cells
AU - Yoo, Seung Jun
AU - Nakra, Neal K.
AU - Ronnett, Gabriele V.
AU - Moon, Cheil
N1 - Publisher Copyright:
© 2014 Korean Endocrine Society.
PY - 2014
Y1 - 2014
N2 - 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.
AB - 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.
KW - Bilirubin
KW - Carbon monoxide
KW - Heme
KW - Iron
KW - Oxygenases
UR - http://www.scopus.com/inward/record.url?scp=84942414471&partnerID=8YFLogxK
U2 - 10.3803/EnM.2014.29.3.356
DO - 10.3803/EnM.2014.29.3.356
M3 - Article
AN - SCOPUS:84942414471
SN - 2093-596X
VL - 29
SP - 356
EP - 362
JO - Endocrinology and Metabolism
JF - Endocrinology and Metabolism
IS - 3
ER -
