Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 1. Chemical aspects and biological sources of oxidative stress in the brain

Moniczewski, Andrzej; Gawlik, Maciej; Smaga, Irena; Niedzielska, Ewa; Krzek, Jan; Przegaliński, Edmund; Pera, Joanna; Filip, Małgorzata

doi:10.1016/j.pharep.2014.12.014

Cited by 62 publications

(45 citation statements)

References 90 publications

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“…The sustained activation of GR during chronic stressful condition may decrease PVB expression by sensitizing interneuron activation and, possibly, through a toxic effect due to NO release. Indeed, NO may be converted in different reactive nitrogen species, thus leading to oxidative damage of proteins, lipids, and DNA that are able to alter neuronal homeostasis (Moniczewski et al, 2015). We also showed that prolonged stress exposure alters the NRF2-KEAP-antioxidant responsive element system, a master regulator of the antioxidative response (Sandberg et al, 2014), with a decrease of NRF2 expression that may impair the activation of antioxidant mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…In the present work we used the chronic mild stress (CMS) model (Willner, 2017) to investigate the detrimental effects of stress on PVB+ cells in rat hippocampus and the potential contribution of a dysregulation in redox mechanisms, which have also been associated with the pathophysiology of several psychiatric disorders (Moniczewski et al, 2015; Smaga et al, 2015; Steullet et al, 2017). We have previously shown that CMS is able to induce depressive-like behaviors such as anhedonia (Rossetti et al, 2016) as well as cognitive impairment (Calabrese et al, 2017), which are associated with alterations in key molecular players for psychiatric disorders (Luoni et al, 2014; Calabrese et al, 2016b; Molteni et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

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Chronic Stress Exposure Reduces Parvalbumin Expression in the Rat Hippocampus through an Imbalance of Redox Mechanisms: Restorative Effect of the Antipsychotic Lurasidone

Rossetti

Paladini

Colombo

et al. 2018

International Journal of Neuropsychopharmacology

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BackgroundPsychiatric disorders are associated with altered function of inhibitory neurotransmission within the limbic system, which may be due to the vulnerability of selective neuronal subtypes to challenging environmental conditions, such as stress. In this context, parvalbumin-positive GABAergic interneurons, which are critically involved in processing complex cognitive tasks, are particularly vulnerable to stress exposure, an effect that may be the consequence of dysregulated redox mechanisms.MethodsAdult Male Wistar rats were subjected to the chronic mild stress procedure for 7 weeks. After 2 weeks, both control and stress groups were further divided into matched subgroups to receive chronic administration of vehicle or lurasidone (3 mg/kg/d) for the subsequent 5 weeks. Using real-time RT-PCR and western blot, we investigated the expression of GABAergic interneuron markers and the levels of key mediators of the oxidative balance in the dorsal and ventral hippocampus.ResultsChronic mild stress induced a specific decrease of parvalbumin expression in the dorsal hippocampus, an effect normalized by lurasidone treatment. Interestingly, the regulation of parvalbumin levels was correlated to the modulation of the antioxidant master regulator NRF2 and its chaperon protein KEAP1, which were also modulated by pharmacological intervention.ConclusionsOur findings suggest that the susceptibility of parvalbumin neurons to stress may represent a key mechanism contributing to functional and structural impairments in specific brain regions relevant for psychiatric disorders. Moreover, we provide new insights on the mechanism of action of lurasidone, demonstrating that its chronic treatment normalizes chronic mild stress-induced parvalbumin alterations, possibly by potentiating antioxidant mechanisms, which may ameliorate specific functions that are deteriorated in psychiatric patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic Stress Exposure Reduces Parvalbumin Expression in the Rat Hippocampus through an Imbalance of Redox Mechanisms: Restorative Effect of the Antipsychotic Lurasidone

Rossetti

Paladini

Colombo

et al. 2018

International Journal of Neuropsychopharmacology

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“…The etiology of depression is multifactorial and related to disturbed monoaminergic transmission, changes in receptor function, dysregulation of the stress axis, a reduction of neurogenesis, activated inflammatory processes, or increased oxidative stress (Moniczewski et al 2015; Smaga et al 2015). Recent observations strongly support the involvement of the endocannabinoid (eCB) system in the pathogenesis of depression.…”

Section: Introductionmentioning

confidence: 99%

Changes in the Brain Endocannabinoid System in Rat Models of Depression

et al. 2017

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A growing body of evidence implicates the endocannabinoid (eCB) system in the pathophysiology of depression. The aim of this study was to investigate the influence of changes in the eCB system, such as levels of neuromodulators, eCB synthesizing and degrading enzymes, and cannabinoid (CB) receptors, in different brain structures in animal models of depression using behavioral and biochemical analyses. Both models used, i.e., bulbectomized (OBX) and Wistar Kyoto (WKY) rats, were characterized at the behavioral level by increased immobility time. In the OBX rats, anandamide (AEA) levels were decreased in the prefrontal cortex, hippocampus, and striatum and increased in the nucleus accumbens, while 2-arachidonoylglycerol (2-AG) levels were increased in the prefrontal cortex and decreased in the nucleus accumbens with parallel changes in the expression of eCB metabolizing enzymes in several structures. It was also observed that CB1 receptor expression decreased in the hippocampus, dorsal striatum, and nucleus accumbens, and CB2 receptor expression decreased in the prefrontal cortex and hippocampus. In WKY rats, the levels of eCBs were reduced in the prefrontal cortex (2-AG) and dorsal striatum (AEA) and increased in the prefrontal cortex (AEA) with different changes in the expression of eCB metabolizing enzymes, while the CB1 receptor density was increased in several brain regions. These findings suggest that dysregulation in the eCB system is implicated in the pathogenesis of depression, although neurochemical changes were linked to the particular brain structure and the factor inducing depression (surgical removal of the olfactory bulbs vs. genetic modulation).

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“…In the complete glucose oxidation process by cells are involved various metabolic pathways (glycolysis, Krebs cycle and the electron transport chain (ETC)) and some cellular compartments (cytoplasm, membrane and mitochondrial matrix). Under physiological conditions, the enzymes of the mitochondrial respiratory chain, as a result of metabolism, are responsible for a constant endogenous production of free radicals (such as reactive oxygen intermediates (ROI) and reactive nitrogen species (RNS)) [28]. The main source of ROS generation is the electron transport chain (ETC) in the mitochondria.…”

Section: Ros (Reactive Oxygen Species)mentioning

confidence: 99%

Altered Inflammatory Mediators in Fibromyalgia

Garcı́a¹,

Carvajal-Gil²,

Herrero-Olea³

et al. 2017

Rheumatology

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Fibromyalgia (FM) is a syndrome characterized by widespread chronic pain, tenderness, stiffness, fatigue, and sleep and mood disturbances. Current evidences suggest that inflammatory mediators may have an important role in the pathogenesis of fibromyalgia. Every day new evidences emerging of the role of the immune system and the inflammatory process in the pathophysiology of this disease. Thus, the aim of this work has been review that altered inductors, inflammatory mediators and effectors have been reported in fibromyalgia, and its relationship to disease's symptoms. If in fibromyalgia underlies widespread disruption of most characteristic components on the inflammatorý s process (endogenous inductors, mediators and effectors) is logical to think that fibromyalgia is producing a sustained inflammatory response in time, unregulated, responsible for the disease´s symptoms. Keywords:Fibromyalgia; Inflammation; HMGB1; Age; Inflammasome; Cytokines; Chemokines; Pentraxins; Lipid mediators; Monocytes; Neutrophils FibromyalgiaFibromyalgia (FM) is a chronic disease characterized by a widespread pain, tenderness, stiffness, fatigue, and sleep and mood disturbances. The prevalence of FM in the world ranges between 0.7% and 3.2%. It is more prevalent on women than men with a ratio women/men 20:1 (4.2% prevalence on women compared with 0.2% on men) [1] and it can develop at any age [2].The exact cause of fibromyalgia is unknown, but it has been proposed that the FM is a stress-related disorder that may involve a dysfunction of the hypothalamic-pituitary-adrenal axis (HPA) [3,4]. Thus, adverse life events, such as emotional, physical and sexual abuse on children and adults have been suggested to contribute to the development of FM [5][6][7].Risk factors FM have been the subject of much debate in recent research. There is no doubt that the experience of an abusive relationship, maintained over time, is a stressful situation that could be related to the presence of FM [8,9].Like all physiological systems, the immune system is under the control of the neuro-endocrine system and interacts and works in concert with other regulatory body systems, thus immune cells respond to neuroendocrine signals through specific receptors for hormones, neurotransmitters and neuropeptides. Therefore, dysregulation of the hypothalamic-pituitary-adrenal axis by chronic stress situations necessarily lead to a dysregulation of the immune function. Thus, inflammation is a characteristic process of the immune system, considered a defense response that is induced by infection or trauma. However, inflammation may also be induced by stress and tissue dysfunction in the absence of infection, there is a close relationship between body homeostasis, stress response and inflammation, since inflammation has both a component response to stress as a component defense response. Inflammation and FibromyalgiaIn 2001, Wallace et al. [10] were the first to suggest that inflammatory mediators, such as cytokines, could play a role in fibromyalgia. Prior results...

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Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 1. Chemical aspects and biological sources of oxidative stress in the brain

Cited by 62 publications

References 90 publications

Chronic Stress Exposure Reduces Parvalbumin Expression in the Rat Hippocampus through an Imbalance of Redox Mechanisms: Restorative Effect of the Antipsychotic Lurasidone

Chronic Stress Exposure Reduces Parvalbumin Expression in the Rat Hippocampus through an Imbalance of Redox Mechanisms: Restorative Effect of the Antipsychotic Lurasidone

Changes in the Brain Endocannabinoid System in Rat Models of Depression

Altered Inflammatory Mediators in Fibromyalgia

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