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It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers.

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Increasing numbers of studies indicate that free radicals and their derivatives play a role in some neuropsychiatric disorders, such as depression. The aim of this study was to investigate the activities of antioxidant enzymes, lipid peroxidation and total antioxidant status (TAS) in patients suffering from major depressive disorder (MDD) as compared to healthy controls. Specifically, we wanted to estimate how fluoxetine influences antioxidant defense and lipid peroxidation. Fifty MDD patients and thirty healthy controls participated in the study. Antioxidant enzyme activities and lipid peroxidation levels were measured in erythrocytes, while TAS was measured in plasma. All measurements were taken during an acute depressive episode and then again during depression remission after a three-month fluoxetine treatment. During acute depressive episodes, patients had significantly higher activity levels of antioxidant enzymes, such as copper-zinc superoxide dismutase (SOD1) and catalase (CAT), as compared to healthy controls. Concentrations of malondialdehyde (MDA) were also significantly higher during depressive episodes. Activity levels of glutathione peroxidase (GPx) did not differ significantly between depressed patients and healthy control subjects. Moreover, the plasma total antioxidant status of the depressed patients was decreased in comparison to control subjects. After three months of fluoxetine treatment, the above parameters did not change significantly. Major depressive disorder is accompanied by disturbances in the balance between pro- and anti-oxidative processes; however, these disturbances do not improve in patients in remission after three months of fluoxetine therapy.

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