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Zaparte A.,Pontifical Catholic University of Rio Grande do Sul | Viola T.W.,Pontifical Catholic University of Rio Grande do Sul | Grassi-Oliveira R.,Pontifical Catholic University of Rio Grande do Sul | Grassi-Oliveira R.,Cognitive Neuroscience Research Group GNCD | And 3 more authors.
Psychopharmacology | Year: 2015

Rationale: Preclinical studies have shown that cocaine exposure and withdrawal are associated with cellular oxidative stress damage. However, the impact of crack-cocaine dependence on oxidative stress biomarkers remains unclear. Here, we assessed peripheral oxidative stress and antioxidant defences during two periods of crack-cocaine detoxification treatment and associated these changes with psychological morbidity. Methods: Thirty female inpatients were recruited, and plasma samples were collected at the 4th and 18th days of abstinence; 30 healthy controls were also recruited. Plasma levels of protein carbonyl, protein thiol content, superoxide dismutase (SOD), glutathione peroxidase (GPx), reduced reduced (GSH) and total reactive antioxidant potential (TRAP) were measured by standard methods; the questionnaires Cocaine Selective Severity Assessment, Beck Depressive Inventory and the Addiction Severity Index were applied. Results: We report higher oxidative stress damage after 4 days of detoxification, as shown by increased total thiol content and protein carbonylation when compared with control group and after 18 days of detoxification. After 18 days of treatment, we observed a recovery of the oxidative stress damage and increase of the antioxidant defences, as shown by higher levels of SOD, GPx, GSH and TRAP. There was a positive correlation between protein carbonylation and psychological variables; in contrast, there was a negative correlation between TRAP levels and clinical assessments. Conclusions: Taken together, these results suggest that drug rehabilitation treatment was effective in decreasing oxidative damage represented by the reduction in biological markers, which are closely related to the severity of withdrawal symptoms. © 2014 Springer-Verlag Berlin Heidelberg. Source


Wieck A.,Cognitive Neuroscience Research Group GNCD | Grassi-Oliveira R.,Cognitive Neuroscience Research Group GNCD | Grassi-Oliveira R.,Pontifical Catholic University of Rio Grande do Sul | Hartmann Do Prado C.,Cognitive Neuroscience Research Group GNCD | And 5 more authors.
NeuroImmunoModulation | Year: 2014

Childhood maltreatment has been linked to enhanced vulnerability to psychiatric pathologies in adult life, including post-traumatic stress disorder (PTSD). Previous works have reported cogent neuroendocrine and immune changes related to adult traumatic events (war survivors, refugees, etc.), but little information is known regarding the impact of early-life stress (ELS) in adult physiology. Here, we review the neuroendocrine and immunological changes commonly observed in PTSD, focusing on the long-term implications of ELS. Childhood maltreatment may lead to altered glucocorticoid (GC) secretion, resulting in hypo- or hypercortisolemia, and reciprocal changes in peripheral leukocyte sensitivity to GC. It is believed that these neuroendocrine changes are correlated with the immune imbalance phenomenon (low-grade inflammation), characterized by increased plasma levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and C-reactive protein. Changes in peripheral lymphocyte subsets are also documented, such as a reduction in regulatory T cells and an expansion of activated T cells. The excess of circulating cytokines may thus interfere with key brain neurotransmitter pathways involved in depression and enhanced risk to cardiovascular, respiratory, gastrointestinal, inflammatory and autoimmune diseases. Recent gene-environment and epigenetic findings have indicated potential molecular mechanisms linking ELS, neuroendocrine and immunity in PTSD. © 2014 S. Karger AG, Basel. Source


Wieck A.,Pontifical Catholic University of Rio Grande do Sul | Grassi-Oliveira R.,Pontifical Catholic University of Rio Grande do Sul | Grassi-Oliveira R.,Cognitive Neuroscience Research Group GNCD | do Prado C.H.,Pontifical Catholic University of Rio Grande do Sul | And 7 more authors.
Neuroscience Letters | Year: 2014

Mounting evidence suggests a chronic pro-inflammatory state in individuals with bipolar disorder (BD). Stress exposure is known to exacerbate several inflammatory conditions as well as psychiatric disorders. Here, we analyzed plasma levels of pro-inflammatory cytokines and their soluble receptors to realistic acute psychosocial stress challenge in BD. Thirteen euthymic type 1 BD patients and 15 matched controls underwent the Trier Social Stress Test protocol (TSST). Blood samples were collected before and after TSST and plasma cytokines interleukin IL-2, IL-6, IL-33, and tumor necrosis factor alpha (TNF-α) were measured. In addition TNF-α soluble receptors TNFR1 and TNFR2, and IL-33 soluble receptor sST2 were assessed. Increased IL-33 and reduced sST2 levels were observed in BD subjects as compared to controls, independently of stress exposure. Following TSST, there were higher levels of IL-2 and reduced levels of sTNFR1 in both groups. However, the magnitude change for both cytokines was found higher in controls than BD subjects. Our data suggest that BD patients have differential stress reactivity as compared to controls, possibly related to an immunologic imbalance and failure of regulatory mechanisms. © 2014 Elsevier Ireland Ltd. Source

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