Role of autophagy in the progress of coronary total occlusion.

OBJECTIVE: In this study, we measured the level of autophagy enzyme in patients with coronary artery disease (CAD) and investigated whether the role of autophagy existed in the progress of coronary collateral and coronary total occlusion (TO). METHODS: Overall, 115 participants were included in this study. They were divided into the three groups: group 1: patients had chronic TO (n=49); group 2: patients had acute TO such as myocardial infarction (n=36); and group 3: participants were normal controls (n=30). The enzyme-linked immunosorbent assay (ELISA) kit for autophagy-related protein 5 (ATG5) in the plasma was studied for these three groups. RESULTS: Autophagy levels were significantly different between the groups (13.7±5.3, 11.7±3.4, and 7.5±3 ng/mL, respectively; p<0.001). In the subgroup analysis, we found significant positive correlations between the level of autophagy and Rentrop score in the Group 1 (r=0.463, p<0.001). CONCLUSION: In the present study, autophagy levels were higher in the patients with CAD than in healthy controls. In addition, serum autophagy levels showed a significant positive correlation with the Rentrop score. An increased autophagy level may be considered an important activator and marker of the atherosclerotic inflammatory process in CAD (Tab. 1, Fig. 2, Ref. 20).

Inhibition of platelet function by GSTM1-null human peripheral lymphocytes exposed to benzo(a)pyrene-induced challenge.

Recent epidemiological studies proposed that the glutathione S-transferase (GST) M1-null genotype may contribute to diseases associated with oxidative stress. The genetic polymorphism exhibited by the GSTM1 may be an important factor in risk toward oxidant chemicals. In this study, we investigated the effect of GSTM1-null genotype in lymphocyte and oxidative stress-dependent inhibition of platelet aggregation. To determine whether GSTM1 deficiency is a genetic determinant of cell toxicity toward oxidant chemicals, lymphocytes were incubated in vitro with low levels of benzo(a)pyrene (BaP), cumene hydroperoxide (CumOOH), or trans-stilbene oxide that do not decrease cell viability, and were assessed for oxidative damage and for the lymphocyte-dependent inhibition of platelet response. Malondialdehyde and carbonyl levels, and the oxidation of cisparinaric acid, were used as biomarkers of oxidative stress in lymphocytes. Following stimulation by BaP or CumOOH, when peroxidation-dependent changes in these parameters were compared between the GSTM1-null genotype and the positive genotype, no significant differences were found between the two genotypes. On the other hand, preincubation of the lymphocytes with BaP or CumOOH attenuated their inhibitory action on ADP-induced platelet aggregation. However, our results indicate that lymphocytes of individuals with the GSTM1-null genotype have greater inhibitory activity on platelet function after exposure to BaP, but not CumOOH, although they are not more susceptible to in vitro oxidative stress.