Oxidative damages in chronic inflammation of a mouse autoimmune disease model

Abstract

Reactive oxygen species are generated in many types of inflammation; it is unclear, however, if inflammation leads to oxidative damage of DNA, proteins and lipids within the inflamed tissues. In this study, we used mice that are homozygous for the alymphoplasia ( aly) mutation as a model to determine if inflammation induces oxidative damage in liver and pancreas. We found that 8-hydroxy-2’-deoxyguanosine (8OHdG), which is a product of oxidative DNA damage, increases with age in livers and pancreata of C57BL/6 aly/aly ( aly/aly) and C57BL/6 wild type (WT) mice. The 8OHdG levels in liver, but not in pancreas, of aged aly/aly mice were significantly higher than those in age-matched WT mice. We showed that aging enhances oxidative protein damage, as measured by carbonylated protein contents, in the pancreata of WT but not aly/aly mice. In contrast, neither aging nor inflammation was associated with lipid damage, as measured by thiobarbituric acid-reactive substances (TBARS), in aly/aly or WT mice. Our results indicate that chronic inflammation in liver but not pancreas leads to increased oxidative damage to DNA, but not to lipids and proteins in aly/aly mouse model.