Is there an oxidative cost of acute stress? Characterization, implication of glucocorticoids and modulation by prior stress experience

Abstract

Acute rises in glucocorticoid hormones allow individuals to adaptively respond to environmental challenges but may also have negative consequences, including oxidative stress. While the effects of chronic glucocorticoid exposure on oxidative stress have been well characterized, those of acute stress or glucocorticoid exposure have mostly been overlooked. We examined the relationship between acute stress exposure, glucocorticoids and oxidative stress in Japanese quail (Coturnix japonica). We (i) characterized the pattern of oxidative stress during an acute stressor in two phenotypically distinct breeds; (ii) determined whether corticosterone ingestion, in the absence of acute stress, increased oxidative stress, which we call glucocorticoid-induced oxidative stress (GiOS); and (iii) explored how prior experience to stressful events affected GiOS. Both breeds exhibited an increase in oxidative stress in response to an acute stressor. Importantly, in the absence of acute stress, ingesting corticosterone caused an acute rise in plasma corticosterone and oxidative stress. Lastly, birds exposed to no previous acute stress or numerous stressful events had high levels of GiOS in response to acute stress, while birds with moderate prior exposure did not. Together, these findings suggest that an acute stress response results in GiOS, but prior experience to stressors may modulate that oxidative cost.

Serum heme oxygenase-1 measurement is useful for evaluating disease activity and outcomes in patients with acute respiratory distress syndrome and acute exacerbation of interstitial lung disease

“…Also, retrospective data derived from AE-IPF patients treated with corticosteroid alone did not show any reduction in mortality rate over the short term [ 39 ]. Several evidence in the animal models suggest that corticosteroid exposure can cause to increase oxidative stress [ 40 , 41 ]. Although the exact mechanism by which corticosteroid increase oxidative stress is not well known, several hypothesis have been reported that glucocorticoids could bind to mitochondrial glucocorticoid receptors and activate mitochondrial function to generate ROS or ROS is generated by the activation of the protein kinase C (PKC) β / p66 shc signaling pathway by glucocorticoid in the cell [ 40 , 41 ].…”

“…Several evidence in the animal models suggest that corticosteroid exposure can cause to increase oxidative stress [ 40 , 41 ]. Although the exact mechanism by which corticosteroid increase oxidative stress is not well known, several hypothesis have been reported that glucocorticoids could bind to mitochondrial glucocorticoid receptors and activate mitochondrial function to generate ROS or ROS is generated by the activation of the protein kinase C (PKC) β / p66 shc signaling pathway by glucocorticoid in the cell [ 40 , 41 ]. Therefore, in patients with ARDS and AE-ILDs, the use of corticosteroids may be harmful from the point of view of oxidative stress increase, and the potential antioxidant treatment such as N-acetylcysteine needs to be examined in the future [ 42 ].…”

Acute aggressive behavior perturbates the oxidative status of a wild bird independently of testosterone and progesterone

“…An increase of glucocorticoids in the blood stream after aggressive interactions has been reported both in seasonally territorial [e.g., 69] and year-round territorial vertebrates [70,71]. Further, a direct link between glucocorticoids and oxidative stress has previously been reported [72–75], and females seem to be more susceptible to the effects of glucocorticoids on oxidative stress than males [reviewed by 73, but see 76]. Thus, the interaction between glucocorticoids and oxidative status could provide an alternative explanation of our results that we cannot resolve at the moment: aggression may lower OXY concentrations directly as a consequence of an increased metabolism or indirectly via an increase in glucocorticoid concentration, or both.…”

Serum heme oxygenase-1 measurement is useful for evaluating disease activity and outcomes in patients with acute respiratory distress syndrome and acute exacerbation of interstitial lung disease

“…Also, retrospective data derived from AE-IPF patients treated with corticosteroid alone did not show any reduction in mortality rate over the short term (39). Several evidence in the animal models suggest that corticosteroid exposure can cause to increase oxidative stress (40,41). Although the exact mechanism by which corticosteroid increase oxidative stress is not well known.…”

“…Although the exact mechanism by which corticosteroid increase oxidative stress is not well known. several hypothesis have been reported that glucocorticoids could bind to mitochondrial glucocorticoid receptors and activate mitochondrial function to generate ROS or ROS is generated by the activation of the protein kinase C (PKC) β / p66 shc signaling pathway by glucocorticoid in the cell (40,41). Therefore, in patients with ARDS and AE-ILDs, the use of corticosteroids may be harmful from the point of view of oxidative stress increase, and the potential antioxidant treatment such as N-acetylcysteine needs to be examined in the future (42).…”