Increased hepatocellular protein carbonylation in human end-stage alcoholic cirrhosis.

ABSTRACT:

Objective

Oxidative stress is a significant contributing factor in the pathogenesis of alcoholic liver disease (ALD). In the murine models of chronic alcohol consumption, induction of oxidative stress results in increased peroxidation of polyunsaturated fatty acids to form highly reactive electrophilic α/β unsaturated aldehydes that post-translationally modify proteins altering activity. Data are presented here suggesting that oxidative stress and the resulting carbonylation of hepatic proteins is an ongoing process involved in alcohol-induced cirrhosis.

Methods

Using age-matched pooled hepatic tissue obtained from healthy humans and patients with end stage cirrhotic ALD, overall carbonylation was assessed by immunohistochemistry and LC-MS/MS of streptavidin purified hepatic

SUBMITTER: Shearn CT 

PROVIDER: S-EPMC4762037 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature