title: Chronic stress differentially affects antioxidant enzymes and modifies the acute stress response in liver of Wistar rats.
abstract: Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx.
authors.affiliation: Laboratory of Molecular Biology and Endocrinology, VINCA Institute of Nuclear Sciences, Belgrade, Serbia.
authors.forename: J
authors.initials: J
authors.lastname: Djordjevic
authors.forename: A
authors.initials: A
authors.lastname: Djordjevic
authors.forename: M
authors.initials: M
authors.lastname: Adzic
authors.forename: A
authors.initials: A
authors.lastname: Niciforovic
authors.forename: M B
authors.initials: MB
authors.lastname: Radojcic
mesh_terms: D000208:Acute Disease; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002374:Catalase / Q000378:metabolism*; D002908:Chronic Disease; D003345:Corticosterone / Q000097:blood; D005979:Glutathione Peroxidase / Q000378:metabolism*; D005980:Glutathione Reductase / Q000378:metabolism*; D006861:Hydrogen Peroxide / Q000378:metabolism; D008099:Liver / Q000201:enzymology*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D013312:Stress, Physiological / Q000502:physiology*; D013482:Superoxide Dismutase / Q000378:metabolism*; D000072105:Superoxide Dismutase-1; D000094765:Glutathione Peroxidase GPX1; D000099156:Superoxide Dismutase 2
chemical_list: D001786:Blood Glucose; D002374:Catalase; D003345:Corticosterone; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D006861:Hydrogen Peroxide; D016328:NF-kappa B; D011965:Receptors, Glucocorticoid; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D000094765:Glutathione Peroxidase GPX1; D000099156:Superoxide Dismutase 2; C000606292:Sod1 protein, rat; C000722069:Gpx1 protein, rat