ObjectiveTo detect the level of oxidative stress markers in serum, including malondialdehyde (MDA), protein carbonyls (PC), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and total antioxidant capacity (TAC), in patients with stable chronic obstructive pulmonary disease (COPD), and explore the impacts of oxidant/antioxidant imbalance in pathogenesis of COPD. MethodsTwo hundred stable COPD patients (the COPD group) and 100 healthy individuals (the control group) were recruited in the study. The concentrations of MDA, PC, 8-OHdG and TAC in serum were detected. Pulmonary function test was performed and the general informations for each subjects were collected. The COPD patients were divided into a smoking subgroup and a non-smoking subgroup, or divided into a mild-moderate airflow limitation subgroup and a severe-extremely severe airflow limitation subgroup. ResultsThe levels of serum MDA, PC and 8-OHdG in the COPD group were significantly higher than those in the control group (all P < 0.01), but the level of serum TAC was significantly lower than that in the control group (P < 0.01). In the COPD patients, the levels of PC and 8-OHdG in the smoking subgroup were significantly higher than those in the non-smoking subgroup (both P < 0.05). The level of PC in the severe-extremely severe airflow limitation subgroup was significantly higher when compared with the mild-moderate airflow limitation subgroup (P < 0.01). Multiple linear regression analysis showed that the levels of PC and 8-OHdG were negatively related with FEV1% pred in the COPD patients, and the PC had greater impacts than 8-OHdG (β=-0.230, -0.219, P < 0.01). ConclusionSmoking can induce the abnormal increase of PC and 8-OHdG in serum which are negatively related with FEV1% pred in COPD patients, which suggests that oxidative stress might play an important role in pathogenesis of COPD.
Reactive oxygen species (ROS) play an important role in the pathogenesis of various cardiovascular diseases, by leading to cell apoptosis and thus causing organic injuries. Anti-ROS therapy is highly anticipated, but currently, there is still no appropriate prevention method. Studies have shown that thioredoxin (Trx), being a kind of significant endogenous antioxidant system, has excellent antioxidant capacity. Promotion of Trx can reduce key biomolecules to eliminate ROS or regulate many signaling pathways, thus resisting ROS injuries, which may be a new anti-ROS strategy. Therefore, we reviewed the research progress of Trx in cardiac antioxidant therapy to discuss its potential and possibility to be a target for prevention of heart-related ROS injury.