Arachidonic Acid and Nitroarachidonic: Effects on NADPH Oxidase Activity

González-Perilli, Lucía; Prolo, Carolina; Álvarez, María Noel

doi:10.1007/978-3-030-11488-6_6

Cited by 11 publications

(8 citation statements)

References 103 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, it is well known that sepsis and septic shock leads to an augmentation of free radical oxygen species, potentially causing increased damage to the host ( 33 ). It is proposed that arachidonic acid and its derivatives may have antagonistic roles on NOX2 activity ( 45 ), advocating the use of vitamin C. In our study, we observed that vitamin C attenuated oxidative burst in monocytes and granulocytes by 14% and 19%, respectively, whereas hydrocortisone attenuated burst in granulocytes by 16%. Among all different inflammatory readouts explored, reduction of oxidative burst by vitamin C was the only significantly affected read-out.…”

Section: Discussionsupporting

confidence: 50%

“…derivatives may have antagonistic roles on NOX2 activity (45), advocating the use of vitamin C. In our study, we observed that vitamin C attenuated oxidative burst in monocytes and granulocytes by 14% and 19%, respectively, whereas hydrocortisone attenuated burst in granulocytes by 16%. Among all different inflammatory readouts explored, reduction of oxidative burst by vitamin C was the only significantly affected read-out.…”

Section: Discussionsupporting

confidence: 48%

See 1 more Smart Citation

Vitamin C, Hydrocortisone, and the Combination Thereof Significantly Inhibited Two of Nine Inflammatory Markers Induced by Escherichia Coli But Not by Staphylococcus Aureus – When Incubated in Human Whole Blood

Medeiros

Schjalm

Christiansen

et al. 2021

Shock

View full text Add to dashboard Cite

Vitamin C combined with hydrocortisone is increasingly being used to treat septic patients, even though this treatment regimen is based on questionable evidence. When used, a marked effect on key players of innate immunity would be expected, as sepsis is featured by a dysregulated immune response. Here, we explored the effect of vitamin C and hydrocortisone alone and combined, in an ex vivo human whole-blood model of Escherichia coli - or Staphylococcus aureus -induced inflammation. Inflammatory markers for activation of complement (terminal C5b-9 complement complex [TCC]), granulocytes (myeloperoxidase), platelets (β-thromboglobulin), cytokines (tumor necrosis factor [TNF], IL-1β, IL6, and IL-8), and leukocytes (CD11b and oxidative burst) were quantified, by enzyme-linked immunosorbent assay, multiplex technology, and flow cytometry. In E. coli - and S. aureus -stimulated whole blood, a broad dose-titration of vitamin C and hydrocortisone alone did not lead to dose–response effects for the central innate immune mediators TCC and IL-6. Hence, the clinically relevant doses were used further. Compared to the untreated control sample, two of the nine biomarkers induced by E. coli were reduced by hydrocortisone and/or vitamin C. TNF was reduced by hydrocortisone alone (19%, P = 0.01) and by the combination (31%, P = 0.01). The oxidative burst of monocytes and granulocytes was reduced for both drugs alone and their combination, (ranging 8–19%, P < 0.05). Using S. aureus , neither of the drugs, alone nor in combination, had any effects on the nine biomarkers. In conclusion, despite the limitation of the ex vivo model, the effect of vitamin C and hydrocortisone on bacteria-induced inflammatory response in human whole blood is limited and following the clinical data.

show abstract

Section: Discussionsupporting

confidence: 50%

Section: Discussionsupporting

confidence: 48%

Vitamin C, Hydrocortisone, and the Combination Thereof Significantly Inhibited Two of Nine Inflammatory Markers Induced by Escherichia Coli But Not by Staphylococcus Aureus – When Incubated in Human Whole Blood

Medeiros

Schjalm

Christiansen

et al. 2021

Shock

View full text Add to dashboard Cite

show abstract

“…In this study figure 2A clearly reveals animals previously treated with MJ33 significantly decreased BthTx-II-induced edema. Besides that, our results suggest that AA generation is intricately linked to increased oxidative stress, since it is a strong regulator of NOXs activity [8,50]. Furthermore, PRDX6 plays an important role mediating edema early stages through another route that would reinforce the oxidative stress during edema.…”

Section: Discussionmentioning

confidence: 65%

Evaluation of Thiol-dependent Enzymes on the Pharmacological Effects Induced by the Catalytically Active PLA2 from Bothrops jararacussu

Toyama¹,

Crc²,

Mn³

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: Clinical cases reports with snake accidents show that venom bite induces increased oxidative stress including several markers of lipid peroxidation and other oxidative stress marker in plasma. Methods: The main findings of this work were performed with BthTx-II on paw edema of animals treated with the toxin and biochemical measurement of COX-2, PGE2, MDA and the effects of peroxiredoxin inhibitors on edema and myotoxicity were also evaluated. Results: The results show that edema and myotoxocity induced by PLA2 (BthTx-II) induces a strong mobilization of arachidonic acid and an increase in cellular oxidative stress as measured by increased malondialdehydo (MDA) concentration and protein carbonylation. Thus, these findings establish the strong link between oxidative stress, arachidonic acid mobilization and that these events may explain the presence of oxidative stress markers in snake-bitten patients. Experiments performed with animals previously treated with commercially purchased inhibitors showed enzymes such as thioredoxin (TXN), thioredoxin reductase (TXNRD) and other glutathione (GSH)-related antioxidant defenses could play an essential role controlling and defining the end of edema on the late phase of PLA2 BthTx-II-induced process. Conclusion. This study showed that thioate-dependent antioxidant enzymes play an important role in resolving the edema induced by BthTx-II.

show abstract

“…Among other activities, AA boosts glutamatergic neurotransmission, stimulates glutamate release, and suppresses its reuptake; its role as a retrograde trans-synaptic messenger in the long-term potentiation (LTP) mechanism has also been postulated [ 11 ]. Free AA can also induce respiratory burst associated with molecular oxygen reduction to superoxide via the activation of the NADPH oxidase complex [ 12 ]. This mechanism may also increase brain cell death, which is of key significance, considering that AA levels are low in cells because freely accumulated AA induces apoptotic processes connected with changes in membrane plasticity and oxidative stress [ 13 ].…”

Section: Arachidonic Acid: An Overviewmentioning

confidence: 99%

The Emerging Role of the Double-Edged Impact of Arachidonic Acid- Derived Eicosanoids in the Neuroinflammatory Background of Depression.

Regulska

Szuster-Głuszczak

Trojan

et al. 2020

View full text Add to dashboard Cite

: Eicosanoids are arachidonic acid (AA) derivatives belonging to a family of lipid signalling mediators that are engaged in both physiological and pathological processes in the brain. Recently, their implication in the prolonged inflammatory response has become a focus of particular interest because, in contrast to acute inflammation, chronic inflammatory processes within the central nervous system (CNS) are crucial for the development of brain pathologies including depression. The synthesis of eicosanoids is catalysed primarily by cyclooxygenases (COX), which are involved in the production of proinflammatory AA metabolites, including prostaglandins and thromboxanes. Moreover, eicosanoid synthesis is catalysed by lipoxygenases (LOXs), which generate both leukotrienes and anti-inflammatory derivatives such as lipoxins. Thus, AA metabolites have double-edged pro-inflammatory and anti-inflammatory, pro-resolving properties, and an imbalance between these metabolites has been proposed as a contributor or even the basis for chronic neuroinflammatory effects. This review focuses on important evidence regarding eicosanoid-related pathways (with special emphasis on prostaglandins and lipoxins) that has added a new layer of complexity to the idea of targeting the double-edged AA-derivative pathways for therapeutic benefits in depression. We also sought to explore future research directions that can support a pro-resolving response to control the balance between eicosanoids and thus to reduce the chronic neuroinflammation that underlies at least a portion of depressive disorders.

show abstract

Arachidonic Acid and Nitroarachidonic: Effects on NADPH Oxidase Activity

Cited by 11 publications

References 103 publications

Vitamin C, Hydrocortisone, and the Combination Thereof Significantly Inhibited Two of Nine Inflammatory Markers Induced by Escherichia Coli But Not by Staphylococcus Aureus – When Incubated in Human Whole Blood

Vitamin C, Hydrocortisone, and the Combination Thereof Significantly Inhibited Two of Nine Inflammatory Markers Induced by Escherichia Coli But Not by Staphylococcus Aureus – When Incubated in Human Whole Blood

Evaluation of Thiol-dependent Enzymes on the Pharmacological Effects Induced by the Catalytically Active PLA2 from Bothrops jararacussu

The Emerging Role of the Double-Edged Impact of Arachidonic Acid- Derived Eicosanoids in the Neuroinflammatory Background of Depression.

Contact Info

Product

Resources

About