| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10738043 | Free Radical Biology and Medicine | 2012 | 10 Pages |
Abstract
⺠This study investigates the role of iNOS in fatty liver graft failure. ⺠iNOS expression and reactive nitrogen species increase markedly in fatty grafts. ⺠iNOS inhibition attenuates injury and improves survival of fatty liver grafts. ⺠iNOS inhibition prevents JNK activation and mitochondrial depolarization. ⺠Mitochondrial depolarization in fatty liver grafts is not due to UCP2 upregulation.
Keywords
MPTTNFαeNOSJnkRh123hpfUCPDepolarizationRNSNOSALTiNOSc-Jun N-terminal kinaseI/RROSAlanine aminotransferaseAlcoholmitochondrial permeability transitionischemia/reperfusionSteatosistumor necrosis factor-αTUNELUW solutionRhodamine 123inducible nitric oxide synthaseendothelial nitric oxide synthaseterminal deoxynucleotidyl transferase-mediated dUTP nick-end labelingMitochondrialhigh power fieldNitric oxidenitric oxide synthaseUncoupling proteinPropidium iodideTransplantationLiver transplantationLiverreactive nitrogen speciesReactive oxygen species
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Authors
Qinlong Liu, Hasibur Rehman, Yasodha Krishnasamy, Venkat K. Ramshesh, Tom P. Theruvath, Kenneth D. Chavin, Rick G. Schnellmann, John J. Lemasters, Zhi Zhong,