Oxidant/antioxidant imbalance is an inherent feature of depression

Abstract

Background50% to 60% of the people who have recovered from the first episode of depression experience a relapse. The immune system of the people suffering from depression is in a permanent state of pathological pro-inflammatory readiness. There are some reports that depressive episodes cause sensitization of immune-inflammatory pathways and that staing of depression (e.g. number of depressive episodes) is correlated with immune-inflammatory markers.The main objective of the study was to delineate whether recurrent major depression (rDD) is characterized by alterations in selected immune-inflammatory biomarkers as compared with first episode of depression (ED-I), i.e. expression of mRNA and enzymatic activity of manganese superoxide dismutase (MnSOD, SOD-2), myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS, NOS-2), and cyclooxygenase-2 (COX-2).MethodsThe study was carried out in a group of 131 patients: ED-I group – 42 patients, rDD group – 89 patients. Depression severity was assessed with the 17-item Hamilton Depression Rating Scale (HDRS). The number of depression episodes and the disease duration periods were recorded in each patient. For the patients, HDRS was administered at admission during the symptomatic phase, which would generally be either before or shortly after modification of the previous antidepressant drug regimen. Reassessment of the mental condition was conducted after 8 weeks of the pharmacological treatment also with the use of the HDRS scale.ResultsNo significant statistical differences were found between the analysed groups as regards the intensity of depressive disorders. No differences in the expression of MnSOD, MPO, COX-2 and i-NOS genes on the level of both mRNA and protein were observed between both groups. No significant interrelation was noticed between the number of depression episodes experienced and the expression of selected genes on the mRNA level and protein level.ConclusionsThere is no significant difference in MnSOD, MPO, COX-2 and i-NOS between patients with recurrent depressive disorders and those in a first episode of depression. These findings suggest that these enzymes are trait markers of depression and are not related to staging of depression.

Trigonelline through the Attenuation of Oxidative Stress Exerts Antidepressant- and Anxiolytic-Like Effects in a Mouse Model of Maternal Separation Stress

“…Oxidative stress and oxidant/antioxidant imbalance are involved in the pathophysiology of psychiatric disorders. Antidepressants mitigated the activity of oxidative stress in depressed patients [4]. The level of MDA increased in psychiatric disorders like depression [50,51].…”

“…Literature has been suggested a role for oxidative stress as increasing in nitric oxide (NO) and malondialdehyde (MDA) as well as oxidant/antioxidant imbal- Lorigooini ance in the pathophysiology of psychiatric disorders like depression and anxiety [4][5][6][7]. Oxidative stress that occurs as a result of stimulating the production of free radicals, nonradical molecules, reactive oxygen, and nitrogen species is involved in depression and anxiety disorders [8].…”

Selenium and manganese in depression – preclinical and clinical studies

“…For instance, a Polish study reported that the enzyme activity of MnSOD was more decreased in patients with recurrent depressive disorders than that in a group of healthy subjects [53]. Nevertheless, no significant interrelation in the expression of this enzyme was found in both groups with the first episode of depression and with recurrent depressive disorders [54].…”

Immune to happiness – inflammatory process indicators and depressive personality traits

“…A new understanding of mood disorders, including depressive disorders, has emerged over the past three decades. Depression is conceptualized as an immune-inflammatory and oxidative stress disorder associated with neuroprogressive changes as a consequence of peripherally activated immune-inflammatory pathways, including peripheral cytokines and immune cells which penetrate into the brain via the blood barrier [6,7], as well as nitro-oxidative stress and antioxidant imbalances [8,9].…”