In particular, a pattern for liver oxidative stress matched the metabolite profile for captopril treatment, but not that for lisinopril, in keeping with the literature recognizing liver injury as a risk for captopril [ 47, 64] but almost never seen for lisinopril [ 43].
Leducq and colleagues presented evidence for an abnormal pattern of oxidative phosphorylation control that correlated with a transition in mitochondrial permeability and persisted after rewarming [ 23].
Kakoki et al. linked this deleterious effect to an enhanced pattern of oxidative stress [24].
Evidence for oxidative stress was found in the pattern of antioxidant compounds, e.g. glutathione S-transferase, methionine sulfoxide reductase and tocopherol (Additional file 1: Table S6).
However, in addition to total ROS, both of these studies examined multiple biomarkers for oxidative stress and found no common patterns between them.
Kayalar, C., Rosing, J. A. N. & Boyer, P. D. An alternating site sequence for oxidative phosphorylation suggested by measurement of substrate binding patterns and exchange reaction inhibitions.
We found indications that patterns of exposure to selenium and smoking combined with data on genetic variation in genes involved in DNA repair for oxidative damage can be valuable to explore.
One possible explanation for this pattern is elevated oxidative damage to DNA mediated by ROS, as outlined above.
Geometric means for oxidative stress variables were calculated and reported.
