| | Study author/date | Major study findings |
| | Lucca et al., 2009 [38] | Chronic mild psychological stress resulted in significant elevations in superoxide, a reactive oxygen species, in the submitochondrial particles of the prefrontal cortex, cortex, and hippocampus in subjects when compared to controls. The results also demonstrated significant elevations in TBARS, a measure of lipid peroxidation, in the cortex of stressed subjects. |
| | De Pablos et al., 2006 [14] | Induction of chronic variate psychological stress enhanced LPS-induced neuroinflammation in the PFC of stressed subjects when compared to nonstressed LPS-induced subjects and controls. Significant findings included increased microglial activation, levels of DA and its metabolite DOPAC, expression of proinflammatory cytokine mRNA (TNF-α, IL-1β, and IL-6), activation of MAP kinases, and loss of NeuN-positive neurons in the PFC. |
| | Munhoz et al., 2006 [18] | Chronic, unpredictable psychological stress potentiated NF-κB binding activity in the frontal cortex and hippocampus and proinflammatory gene expression of IL-β, TNF-α, and NOS-2 as mediated by elevated GC levels in LPS-induced subjects when compared to controls. |
| | Kim et al., 2005 [41] | Acute psychological stress resulted in elevated BH4 and DA levels in striatal tissues and led to greater lipid peroxidation, protein-bound quinone, neuromelanin, and antioxidant enzyme activities, markers of oxidative stress, in the substantia nigra and striatum of subjects when compared to controls. Furthermore, in subjects exposed to stress, TH-immunoreactive DA neurons demonstrated strong Fluoro-Jade staining, indicating selective degeneration of dopaminergic neurons. In contrast, no Fluoro-Jade staining was identified in controls. |
| | Munhoz et al., 2004 [26] | Repeated psychological stress was associated with time-dependent markers of oxidative stress in brain tissue to include increase in Ca2+-independent NOS-2 activity, lipid peroxidation, TNF-α, and TACE activity in subjects when compared to controls. |
| | Madrigal et al., 2003 [33] | Acute psychological stress was associated with higher levels of PGE2, a marker of COX-2 neuronal activity, MDA and oxidized glutathione, markers of lipid peroxidation, and NOS-2 in the cortex of subjects when compared to controls. |
| | Madrigal et al., 2002 [30] | Acute psychological stress induced the expression of iNOS in the brain cortex, which was preceded by increased expression of TACE and the subsequent release of TNF-α in subjects as compared to controls. Furthermore, the results demonstrated that increased production of TNF-α was involved in stress-induced expression of iNOS as mediated by activation of NF-κB. |
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TBARS, thiobarbituric acid reactive species; LPS, lipopolysaccharide; PFC, prefrontal cortex; DA, dopamine; DOPAC, 3,4-dihydroxyphenylacetic; mRNA, messenger ribonucleic acid; TNF-α, tumor necrosis factor alpha; IL-1β, interleukin-1 beta; IL-6, interleukin-6; MAP, mitogen-activated protein; NeuN-positive, neuronal nuclei positive; GC, glucocorticoids; BH4, tetrahydrobiopterin; TH-immunoreactive, tyrosine hydroxylase; Ca2+, calcium2+; NOS-2, inducible nitric oxide synthase; TACE, TNF-α converting enzyme; iNOS, inducible nitric oxide synthase; PGE2, prostaglandin E2; COX-2, cyclooxygenase-2; MDA, malondialdehyde.
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