Reactive nitrogen species contribute to the rapid onset of redox changes induced by acute immobilization stress in rats

Chen, Hsiao-Jou Cortina, Spiers, Jereme G., Sernia, Conrad, Anderson, Stephen T. and Lavidis, Nickolas A. (2014) Reactive nitrogen species contribute to the rapid onset of redox changes induced by acute immobilization stress in rats. Stress, 17 6: 520-527. doi:10.3109/10253890.2014.966264


Author Chen, Hsiao-Jou Cortina
Spiers, Jereme G.
Sernia, Conrad
Anderson, Stephen T.
Lavidis, Nickolas A.
Title Reactive nitrogen species contribute to the rapid onset of redox changes induced by acute immobilization stress in rats
Journal name Stress   Check publisher's open access policy
ISSN 1025-3890
1607-8888
Publication date 2014-12-01
Year available 2014
Sub-type Article (original research)
DOI 10.3109/10253890.2014.966264
Open Access Status Not yet assessed
Volume 17
Issue 6
Start page 520
End page 527
Total pages 8
Place of publication London, United Kingdom
Publisher Informa Healthcare
Language eng
Subject 2802 Behavioral Neuroscience
2807 Endocrine and Autonomic Systems
1314 Physiology
2738 Psychiatry and Mental health
3206 Neuropsychology and Physiological Psychology
2700 Medicine
Abstract Acute stress leads to the rapid secretion of glucocorticoids, which accelerates cellular metabolism, resulting in increased reactive oxygen and nitrogen species generation. Although the nitrergic system has been implicated in numerous stress-related diseases, the time course and extent of nitrosative changes during acute stress have not been characterized. Outbred male Wistar rats were randomly allocated into control (n = 9) or 120 min acute immobilization stress (n = 9) groups. Serial blood samples were collected at 0 (baseline), 60, 90, and 120 min. Plasma corticosterone concentrations increased by approximately 350% at 60, 90, and 120 (p < 0.001) min of stress. The production of nitric oxide, measured as the benzotriazole form of 4-amino-5-methylamino-2′,7′-difluorofluorescein, increased during stress exposure by approximately 5%, 10%, and 15% at 60 (p < 0.05), 90 (p < 0.01) and 120 (p < 0.001) min, respectively, compared to controls. Nitric oxide metabolism, measured as the stable metabolites nitrite and nitrate, showed a 40-60% increase at 60, 90, and 120 (p < 0.001) min of stress. The oxidative status of 2′,7′-dichlorofluorescein in plasma was significantly elevated at 60 (p < 0.01), 90, and 120 (p < 0.001) min. A delayed decrease of approximately 25% in the glutathione redox ratio at 120 min (p < 0.001) also indicates stress-induced cellular oxidative stress. The peroxidation of plasma lipids increased by approximately 10% at 90 (p < 0.05) and 15% at 120 (p < 0.001) min, indicative of oxidative damage. It was concluded that a single episode of stress causes early and marked changes of both oxidative and nitrosative status sufficient to induce oxidative damage in peripheral tissues.
Formatted abstract
Acute stress leads to the rapid secretion of glucocorticoids, which accelerates cellular metabolism, resulting in increased reactive oxygen and nitrogen species generation. Although the nitrergic system has been implicated in numerous stress-related diseases, the time course and extent of nitrosative changes during acute stress have not been characterized. Outbred male Wistar rats were randomly allocated into control (n=9) or 120 minute acute immobilization stress (n=9) groups. Serial blood samples were collected at 0 (baseline), 60, 90, and 120 minutes. Plasma corticosterone concentrations increased by approximately 350% at 60, 90, and 120 (p<0.001) minutes of stress. The production of nitric oxide,   measured as the benzotriazole form of 4-amino-5-methylamino-2’,7’- difluorofluorescein, increased during stress exposure by approximately 5%, 10%, and 15% at 60 (p<0.05), 90 (p<0.01) and 120 (p<0.001) minutes respectively compared to controls. Nitric oxide metabolism, measured as the stable metabolites nitrite and nitrate, showed a 40% to 60% increase at 60, 90, and 120 (p<0.001) minutes of stress. The oxidative status of 2’, 7’-dichlorofluorescein in plasma was significantly elevated at 60 (p<0.01), 90, and 120 (p<0.001) minutes. A delayed decrease of approximately 25% in the glutathione redox ratio at 120 minutes (p<0.001) also indicates stress-induced cellular oxidative stress. The peroxidation of plasma lipids increased by approximately 10% at 90 (p<0.05) and 15% at 120 (p<0.001) minutes, indicative of oxidative damage. It was concluded that a single episode of stress causes early and marked
Keyword Acute stress
Lipid peroxidation
Nitric oxide
Oxidative stress
Reactive oxygen species
Redox status
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Biomedical Sciences Publications
 
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Created: Sat, 18 Oct 2014, 22:43:48 EST by Jereme Spiers on behalf of School of Biomedical Sciences