Roles of homopolymeric apoferritin in alleviating alcohol-induced liver injury

Abstract

Alcohol abuse induced liver damage are closely related to oxidative stress, several efforts have been made to quench free radicals produced in the liver. Heteropolymeric soybean seed ferritin has been proved to protect DNA from oxidative damage. However, the roles of homopolymeric apoferritin in quenching free radicals have been neglected so far. In order to improve the ferroxidase activity of ferritin, we have prepared apo ferritin by removing iron core from the cavity. In this study, the roles of apo shrimp ferritin (Marsupenaeus japonicus ferritin, MjFer) and human H chain ferritin (HuHF) in attenuating the hydroxyl radicals in vitro and in vivo has been investigated. Results showed that MjFer was able to quench the free radicals produced by iron oxidation more efficiently than HuHF in vitro. Animal studies using a mouse model of alcohol-induced acute liver injury revealed that MjFer is much more efficacious than HuHF in alleviating the liver injury, by attenuating oxidative stress and regulating Nrf2/HO1 expression. Accordingly, the higher activity of MjFer may be attributed to its faster iron oxidative rate than HuHF, which may help improve the intestinal integrity, and reduce abnormal iron absorption. As expected, iron contents in the liver of MjFer and HuHF group are much lower than that of model group, further alleviating the liver damage. These findings suggest that apoferritin may be a promising candidate for alcohol-induced liver injury.