Urine 3-Nitrotyrosine and Serum HDL as Potential Biomarkers of Depression

Nobis, Aleksander; Samaryn, Eliza; Maciejczyk, Mateusz; Waszkiewicz, Napoleon

doi:10.3390/jcm12010377

Cited by 5 publications

(3 citation statements)

References 67 publications

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“…It is related to the excessive activation of the enzyme indole 2,3-dioxygenase (IDO) catabolizing tryptophan to kynurenine and its metabolites [17]. Nevertheless, a study presented by Nobis et al showed similar results to the current study [66]. It can be only theorized that the increased levels of TRY in depressed patients may derive from the catabolic degradation of body proteins at the onset of depression/inflammation and TRY release.…”

Section: Discussionsupporting

confidence: 69%

The Effect of Antidepressant Treatment on Neurocognitive Functions, Redox and Inflammatory Parameters in the Context of COVID-19

Samaryn,

Galińska-Skok,

Nobis

et al. 2023

JCM

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Inflammation is an important component of the etiopathology of depression that uses oxidative and nitrosative stress (O&NS) and elevated inflammatory markers. SARS-CoV-2 infection is also associated with abnormal inflammatory processes, which may impair effective treatment of depression in COVID-19 survivors. In the presented study, thirty-three hospitalized patients with major depressive disorder (MDD) were started on antidepressant treatment, and twenty-one were re-evaluated after 4–6 weeks. The control group consisted of thirty healthy volunteers. All participants underwent neuropsychiatric evaluation, biochemical blood and urine analyses. The results of the research demonstrated positive correlations of the Hamilton Depression Rating Scale (HAM-D) scores with serum catalase (CAT) and urinary S-Nitrosothiols levels, and the Beck Depression Inventory (BDI) scores with serum reduced glutathione (GSH) and superoxide dismutase (SOD) levels. Depressed patients with a history of COVID-19 prior to the treatment had higher urinary nitric oxide (NO) levels and lower serum glutathione peroxidase (GPx) levels. In the control group, COVID-19 survivors had higher levels of urinary N-formylkynurenine (NFK). Our results suggest that the antidepressant treatment has a modulating effect on O&NS, reduces depressive symptoms and improves cognitive functions The present study does not indicate that clinical response to antidepressant treatment is associated with COVID-19 history and baseline SARS-CoV-2 antibody levels. Nevertheless, further research in this area is needed to systematize antidepressant treatment in COVID-19 survivors.

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Section: Discussionsupporting

confidence: 69%

The Effect of Antidepressant Treatment on Neurocognitive Functions, Redox and Inflammatory Parameters in the Context of COVID-19

Samaryn,

Galińska-Skok,

Nobis

et al. 2023

JCM

Self Cite

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“…In our recent work (22), we posited that the causal marker of oxidative stress in adolescents with depressive disorder is NT. Nobis et al (40) found a decreased level of TRP and an increased level of NT in the urine of adult depressive patients by our results in children and adolescents. This supports our assertion that nitrosative stress also plays a role in the pathophysiology of depressive disorder (41).…”

Section: Metabolitesupporting

confidence: 68%

The kynurenine and serotonin pathway, neopterin and biopterin in depressed children and adolescents: an impact of omega-3 fatty acids, and association with markers related to depressive disorder. A randomized, blinded, prospective study

Ilavská,

Morvová,

Paduchová

et al. 2024

Front. Psychiatry

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Depressive disorder is a severe mental condition. In addition to genetic factors, immunological-inflammatory factors, oxidative stress, and disturbances in neurotransmitter metabolism, kynurenine and serotonin pathways may play a role. The exact mechanisms, especially in depressed children and adolescents, are not fully understood. Our primary hypothesis was whether the metabolites of tryptophan degradation in children and adolescents with depressive disorder might be influenced by omega-3 FAs compared to omega-6 FAs during a 12-week supplementation. A secondary hypothesis was to investigate whether tryptophan metabolites in children and adolescents are associated with markers of inflammatory response, oxidative stress, cortisol, and the serum omega-6/omega-3 FA ratio. Metabolites of tryptophan degradation and pteridines, neopterin, and biopterin in urine were analyzed with an HPLC system. Surprisingly, omega-3 FAs stimulated both kynurenine (kynurenine/tryptophan ratio) and serotonin (5-hydroxytryptophan) pathways, whereas omega-6 FAs only increased the kynurenine/tryptophan ratio. Neopterin and biopterin were not different from the healthy controls. Biopterin increased after omega-3 FA supplementation. Serotonin was positively correlated with lipoperoxidation and a marker of oxidative protein damage. Of the monitored tryptophan metabolites, only 5-hydroxyindolacetic acid was positively correlated with the severity of depression, total cholesterol, and negatively with brain-derived neurotrophic factor and glutathione peroxidase. In conclusion, in children and adolescents, both supplemented FAs stimulated the kynurenine pathway (kynurenine/tryptophan ratio) and kynurenine formation. However, the serotonin pathway (5-hydroxytryptophan) was stimulated only by omega-3 FA. Tryptophan metabolism is associated with oxidative stress, inflammation, total cholesterol, and cortisol. We are the first to point out the association between the kynurenine pathway (KYN/TRP ratio) and the omega-6/omega-3 FA ratio. The metabolite 5-HIAA could play a role in the pathophysiology of depressive disorder in children and adolescents.Clinical Trial Registrationhttps://www.isrctn.com/ISRCTN81655012, identifier ISRCTN81655012.

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“…ONOO − nitrates tyrosine residues on proteins, generating 3-nitrotyrosine (3-NT), a biomarker of NO-dependent nitrosative stress. Urine levels of 3-NT are higher in depressed compared to non-depressed patients, implying that nitrosative stress is a major contributor to cytokine induced depression (115).…”

Section: Reactive Nitrogen Speciesmentioning

confidence: 98%

Chronic stress, neuroinflammation, and depression: an overview of pathophysiological mechanisms and emerging anti-inflammatories

Hassamal

2023

Front. Psychiatry

105

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In a subset of patients, chronic exposure to stress is an etiological risk factor for neuroinflammation and depression. Neuroinflammation affects up to 27% of patients with MDD and is associated with a more severe, chronic, and treatment-resistant trajectory. Inflammation is not unique to depression and has transdiagnostic effects suggesting a shared etiological risk factor underlying psychopathologies and metabolic disorders. Research supports an association but not necessarily a causation with depression. Putative mechanisms link chronic stress to dysregulation of the HPA axis and immune cell glucocorticoid resistance resulting in hyperactivation of the peripheral immune system. The chronic extracellular release of DAMPs and immune cell DAMP-PRR signaling creates a feed forward loop that accelerates peripheral and central inflammation. Higher plasma levels of inflammatory cytokines, most consistently interleukin IL-1β, IL-6, and TNF-α, are correlated with greater depressive symptomatology. Cytokines sensitize the HPA axis, disrupt the negative feedback loop, and further propagate inflammatory reactions. Peripheral inflammation exacerbates central inflammation (neuroinflammation) through several mechanisms including disruption of the blood–brain barrier, immune cellular trafficking, and activation of glial cells. Activated glial cells release cytokines, chemokines, and reactive oxygen and nitrogen species into the extra-synaptic space dysregulating neurotransmitter systems, imbalancing the excitatory to inhibitory ratio, and disrupting neural circuitry plasticity and adaptation. In particular, microglial activation and toxicity plays a central role in the pathophysiology of neuroinflammation. Magnetic resonance imaging (MRI) studies most consistently show reduced hippocampal volumes. Neural circuitry dysfunction such as hypoactivation between the ventral striatum and the ventromedial prefrontal cortex underlies the melancholic phenotype of depression. Chronic administration of monoamine-based antidepressants counters the inflammatory response, but with a delayed therapeutic onset. Therapeutics targeting cell mediated immunity, generalized and specific inflammatory signaling pathways, and nitro-oxidative stress have enormous potential to advance the treatment landscape. Future clinical trials will need to include immune system perturbations as biomarker outcome measures to facilitate novel antidepressant development. In this overview, we explore the inflammatory correlates of depression and elucidate pathomechanisms to facilitate the development of novel biomarkers and therapeutics.

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Urine 3-Nitrotyrosine and Serum HDL as Potential Biomarkers of Depression

Cited by 5 publications

References 67 publications

The Effect of Antidepressant Treatment on Neurocognitive Functions, Redox and Inflammatory Parameters in the Context of COVID-19

The Effect of Antidepressant Treatment on Neurocognitive Functions, Redox and Inflammatory Parameters in the Context of COVID-19

The kynurenine and serotonin pathway, neopterin and biopterin in depressed children and adolescents: an impact of omega-3 fatty acids, and association with markers related to depressive disorder. A randomized, blinded, prospective study

Chronic stress, neuroinflammation, and depression: an overview of pathophysiological mechanisms and emerging anti-inflammatories

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