The impact of chronic stress on intracellular redox balance: A systems level analysis

Abstract

Chronic psychosocial stress is implicated in the onset and progression of noncommunicable diseases, and mechanisms underlying this relationship include alterations to the intracellular redox state. However, such changes are often investigated in isolation, with few studies adopting a system level approach. Here, male Wistar rats were exposed to 9.5 weeks of chronic unpredictable mild stress and redox status assays were subsequently performed on cardiac, hepatic, and brain tissues versus matched controls. The stressed rats displayed an anxious phenotype, with lowered plasma corticosterone levels (p = 0.04 vs. Controls) and higher plasma epinephrine concentrations (p = 0.03 vs. Controls). Our findings showed organ‐specific redox profiles, with stressed rats displaying increased myocardial lipid peroxidation (p = 0.04 vs. Controls) in the presence of elevated nonenzymatic antioxidant capacity (p = 0.04 vs. Controls). Conversely, hepatic tissues of stressed rats exhibited lowered nonenzymatic antioxidant capacity (p < 0.001 vs. Controls) together with increased superoxide dismutase (SOD) activity (p = 0.05 vs. Controls). The brain displayed region‐specific antioxidant perturbations, with increased SOD activity (p = 0.01 vs. Controls) in the prefrontal cortex of the stressed rats. These findings reveal distinct stress‐related organ‐specific vulnerability to redox perturbations and may provide novel insights into putative therapeutic targets.

Angelica keiskeileaves extract attenuates psychosocial stress in overcrowding-subjected rats

“…Long-term exposure to psychosocial stress can induce enormous reactive oxygen species (ROS) and oxidative damage, triggering various cellular responses such as neurodegeneration, tissue damage, and cell death that are responsible for the depressive symptoms [12,44]. A study reported that chronic psychosocial stress causes redox perturbations in the brain tissue of rats [45]. In the present study, MDA and SOD were used as oxidative stress markers.…”