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Article: Carbon monoxide inhalation rescues mice from fulminant hepatitis through improving hepatic energy metabolism

TitleCarbon monoxide inhalation rescues mice from fulminant hepatitis through improving hepatic energy metabolism
Authors
KeywordsApoptosis
Carbon monoxide
Energy metabolism
Fulminant hepatitis
Soluble guanylyl cyclase
Issue Date2007
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.shockjournal.org
Citation
Shock, 2007, v. 27 n. 2, p. 165-171 How to Cite?
AbstractHeme oxygenase 1 (HO-1) enhances cellular antioxidative capability by increasing the cleavage of the endogenous and exogenous heme. Besides the biochemical activities of HO, the products of heme degradation significantly contribute to the cytoprotective effects of HO. Here, we show that HO-1 deficiency significantly increases the susceptibility of mice to apoptotic insults, whereas expression of HO-1 significantly increased the resistance of primary hepatocyte to apoptosis. This phenomenon was correlated with the production of one of its catalytic products-carbon monoxide (CO). Surprisingly, exposing the primary mouse hepatocyte to CO could improve the cellular energy metabolism in a soluble guanylyl cyclase-dependent manner. One-hour inhalation of low-dose CO enhanced the hepatic soluble guanylyl cyclase activities in mice. In parallel, the levels of hepatic adenosine triphosphate increased significantly and were associated with a marked reduction of TNF-α-induced apoptosis in the liver of D-galactosamine-sensitized mice. In addition, CO inhalation for 1 h significantly improved the survival of mice after initiation of fulminant hepatitis. Up to 90% of mice given CO survived for more than 7 days, whereas control mice died within 12 h. The data provide novel insight of CO-mediated cytoprotection. ©2007The Shock Society.
Persistent Identifierhttp://hdl.handle.net/10722/84015
ISSN
2015 Impact Factor: 3.048
2015 SCImago Journal Rankings: 1.336
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTsui, TYen_HK
dc.contributor.authorObed, Aen_HK
dc.contributor.authorSiu, YTen_HK
dc.contributor.authorYet, SFen_HK
dc.contributor.authorPrantl, Len_HK
dc.contributor.authorSchlitt, HJen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:47:55Z-
dc.date.available2010-09-06T08:47:55Z-
dc.date.issued2007en_HK
dc.identifier.citationShock, 2007, v. 27 n. 2, p. 165-171en_HK
dc.identifier.issn1073-2322en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84015-
dc.description.abstractHeme oxygenase 1 (HO-1) enhances cellular antioxidative capability by increasing the cleavage of the endogenous and exogenous heme. Besides the biochemical activities of HO, the products of heme degradation significantly contribute to the cytoprotective effects of HO. Here, we show that HO-1 deficiency significantly increases the susceptibility of mice to apoptotic insults, whereas expression of HO-1 significantly increased the resistance of primary hepatocyte to apoptosis. This phenomenon was correlated with the production of one of its catalytic products-carbon monoxide (CO). Surprisingly, exposing the primary mouse hepatocyte to CO could improve the cellular energy metabolism in a soluble guanylyl cyclase-dependent manner. One-hour inhalation of low-dose CO enhanced the hepatic soluble guanylyl cyclase activities in mice. In parallel, the levels of hepatic adenosine triphosphate increased significantly and were associated with a marked reduction of TNF-α-induced apoptosis in the liver of D-galactosamine-sensitized mice. In addition, CO inhalation for 1 h significantly improved the survival of mice after initiation of fulminant hepatitis. Up to 90% of mice given CO survived for more than 7 days, whereas control mice died within 12 h. The data provide novel insight of CO-mediated cytoprotection. ©2007The Shock Society.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.shockjournal.orgen_HK
dc.relation.ispartofShocken_HK
dc.rightsShock. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subjectApoptosisen_HK
dc.subjectCarbon monoxideen_HK
dc.subjectEnergy metabolismen_HK
dc.subjectFulminant hepatitisen_HK
dc.subjectSoluble guanylyl cyclaseen_HK
dc.titleCarbon monoxide inhalation rescues mice from fulminant hepatitis through improving hepatic energy metabolismen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1073-2322&volume=27&issue=2&spage=165&epage=171&date=2007&atitle=Carbon+monoxide+inhalation+rescues+mice+from+fulminant+hepatitis+through+improving+hepatic+energy+metabolismen_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/01.shk.0000239781.71516.61en_HK
dc.identifier.pmid17224791-
dc.identifier.scopuseid_2-s2.0-33846237222en_HK
dc.identifier.hkuros125968en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846237222&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issue2en_HK
dc.identifier.spage165en_HK
dc.identifier.epage171en_HK
dc.identifier.isiWOS:000243796400009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTsui, TY=7006622455en_HK
dc.identifier.scopusauthoridObed, A=23009911000en_HK
dc.identifier.scopusauthoridSiu, YT=8953557400en_HK
dc.identifier.scopusauthoridYet, SF=7003871804en_HK
dc.identifier.scopusauthoridPrantl, L=11140839500en_HK
dc.identifier.scopusauthoridSchlitt, HJ=7005572464en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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