Deletion of GSTA4-4 results in increased mitochondrial post-translational modification of proteins by reactive aldehydes following chronic ethanol consumption in mice
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- 作者：Colin T. Shearna ; colin.shearn@ucdenver.edu" class="auth_mail" title="E-mail the corresponding author ; Kristofer S. Fritza ; Alisabeth H. Shearnb ; Laura M. Sabaa ; Kelly E. Mercerc ; Bridgette Engic ; James J. Galligane ; Piotr Zimniakc ; David J. Orlickyd ; Martin J. Ronisf ; Dennis R. Petersena ;
- 关键词：ADPH ; adipophilin ; ALD ; alcoholic liver disease ; ALT ; alanine aminotransferase ; CID ; collision-induced dissociation ; Cyp2E1 ; Cytochrome P4502E1 ; ETD ; electron transfer dissociation ; EtOH ; ethanol ; GSTA4 ; glutathione S-transferase isoform A4 ; 4-HHE ; 4-hydroxy-2-hexenal ; 4-HNE ; 4-hydroxy-2-nonenal ; MDA ; malondialdehyde ; 4-ONE ; 4-oxononenal ; PF ; Pair-fed
- 刊名：Redox Biology
- 出版年：2016
- 出版时间：April 2016
- 年：2016
- 卷：7
- 期：Complete
- 页码：68-77
- 全文大小：8622 K
文摘
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We demonstrate increased mitochondrial carbonylation in GSTA4-4 KO mice chronically fed EtOH.
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Using LC-MS we identify 829 total carbonylated proteins (417 novel to murine ALD).
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Pathway analysis revealed a propensity for adduction of fatty acid metabolic and electron transport proteins.
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Using MS/MS, 26 novel adducted peptides were identified.
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Reactive aldehyde modification of proteins contributes to pathogenesis of ALD.