Thiobarbituric Acid-Reactive Substances: Markers of an Acute Episode and a Late Stage of Bipolar Disorder

Abstract

Background: Lowered antioxidant defense systems and increased oxidative stress are implicated in bipolar disorders (BD). Early and late stages of BD may present different biological features (including the level of oxidative stress) and may therefore require different treatment strategies. The aim of this study was to analyze serum levels of lipid peroxidation [measured as thiobarbituric acid-reactive substances (TBARS), a derivative of malondialdehyde] in BD patients at various stages and phases of the illness and compare their TBARS levels with those of healthy controls. Method: A total of 129 patients (58 in the depressive episode, 23 in the manic episode and 48 in remission) diagnosed with type I (n = 69) or type II (n = 60) BD and 50 healthy volunteers (control group) were enrolled in the study. The level of lipid peroxidation was measured in blood serum using a TBARS assay kit. Results: TBARS levels in the acute episode of mania/hypomania and depression (but not in remission) were significantly higher than in healthy controls. With regard to the BD stage, both early- and late-stage BD TBARS levels were significantly increased in patients in the depressive episode. In late-stage BD, the TBARS level in patients in remission remained elevated compared with controls. A multiple regression model confirmed the association between the TBARS level and BD stage or acute BD. Conclusion: Our findings indicate that TBARS levels reflect the oxidative stress state which increases both in the acute phase of BD (mania/hypomania and depression) and with BD progression (stage).

Natural regulatory IgM‐mediated autoimmune responses directed against malondialdehyde regulate oxidative and nitrosative pathways and coupled with IgM responses to nitroso adducts attenuate depressive and physiosomatic symptoms at the end of term pregnancy

“…MDA, in turn, may cause deleterious effects to proteins and DNA thereby exerting neurotoxic effects and promoting cell death . Increased MDA levels in depression and bipolar disorder are now well established and have been consolidated in meta‐analyses …”

“…1,2 MDA, in turn, may cause deleterious effects to proteins and DNA thereby exerting neurotoxic effects and promoting cell death. 3,4 Increased MDA levels in depression and bipolar disorder are now well established [5][6][7][8][9] and have been consolidated in meta-analyses. [10][11][12] MDA is an oxidative-specific epitope (OSE) that is expressed on the cell surface of oxidized low-density lipoprotein (LDL), apoptotic and dying cells, 13 and circulating microparticles (MP).…”

Na+, K+-ATPase Signaling and Bipolar Disorder

“…Reduced antioxidant capacity leads to the accumulation of Reactive oxygen species (ROS), which, in turn, causes oxidative damage to macromolecules. Indeed, biomarkers indicating oxidative damage were reported in BD patients: higher levels of protein carbonylation and lipid peroxidation [26]. In addition to the permanent changes, several studies found a correlation between manic or depressive mood states and the levels of oxidative damage biomarkers in bipolar individuals [26].…”

“…Indeed, biomarkers indicating oxidative damage were reported in BD patients: higher levels of protein carbonylation and lipid peroxidation [26]. In addition to the permanent changes, several studies found a correlation between manic or depressive mood states and the levels of oxidative damage biomarkers in bipolar individuals [26]. In addition, neurotrophic factors, mainly brain-derived neurotrophic factor (BDNF), are important for neuroplasticity, a process that is impaired in patients suffering from BD [27,28], and Wnt and GSK-3 signaling [29] participate in the etiology of the disease.…”

The serum zinc concentration as a potential biological marker in patients with major depressive disorder

“…The presented results are a part of the large clinical study named De-Me-Ter (“Depression – Mechanisms – Therapy”, task 3.2 - Identification of endogenous marker of depression and therapy effectiveness) (Siwek et al 2016a, b; Siwek et al 2015; Styczeń et al 2015). …”