Oxidative Stress Status and its correlation with Redox Status as Measured By An Electrochemical (PAOT®) Methodology: A Pilot Study in Critical COVID-19 Pneumonia Survivors

Choledocholithiasis may cause biliary obstruction which leads to hepatocellular injury. Oxidative stress has been proposed as a possible mechanism involved in this disorder. This study evaluates the oxidative stress burden in patients with choledocholithiasis and secondary cholestasis, before and after endoscopic sphincterotomy. Experimental part: Patients diagnosed with choledocholithiasis and secondary extrahepatic cholestasis were included in the study between January 1st 2016 and October 31st 2016. In all patients oxidative stress markers were collected within 2 hours before and 48 hours after therapeutic ERCP. Selected markers were superoxide dismutase (SOD), glutathione peroxidase (GPX) and malondialdehyde (MDA). The results were compared to those from a group of 40 healthy subjects. Significantly lower concentrations of SOD (p = 0.03) and GPX (p [ 0.0001) activities, associated with an increased level of MDA level (p [ 0.0001) were shown in patients before biliary clearance compared with the healthy control group. After ERCP the only oxidative stress parameter which showed improvement was the SOD specific activity (p = 0.037). This study shows that extrahepatic cholestasis secondary to choledocholithiasis is associated with increased oxidative stress status. After biliary clearance one oxidative stress marker was significantly improved (SOD), suggesting a possible antioxidant effect of such procedure.

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Modulatory Role of Riboceine and Vitamin C Supplementation on Altered Oxidative Stress Status of Alloxan-induced Diabetic Wistar Rats

Bioscience Biotechnology Research Communications ◽

10.21786/bbrc/13.4/75 ◽

2020 ◽

Vol 13 (4) ◽

pp. 2130-2138

Author(s):

Akingbade Bamidele Thomas

Keyword(s):

Oxidative Stress ◽

Vitamin C ◽

Wistar Rats ◽

Oxidative Stress Status ◽

Vitamin C Supplementation

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Oxidative stress status: An introduction

Free Radical Biology and Medicine ◽

10.1016/0891-5849(91)90071-a ◽

1991 ◽

Vol 10 (3-4) ◽

pp. 173 ◽

Cited By ~ 13

Author(s):

William A. Pryor ◽

Susan Shipley Godber

Keyword(s):

Oxidative Stress ◽

Oxidative Stress Status

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Dexamethasone increased the survival rate in Plasmodium berghei-infected mice

Scientific Reports ◽

10.1038/s41598-021-82032-7 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Danilo Reymão Moreira ◽

Ana Carolina Musa Gonçalves Uberti ◽

Antonio Rafael Quadros Gomes ◽

Michelli Erica Souza Ferreira ◽

Aline da Silva Barbosa ◽

...

Keyword(s):

Oxidative Stress ◽

Survival Rate ◽

Plasmodium Berghei ◽

Redox Status ◽

No Synthase ◽

Ischemia And Reperfusion ◽

Inos Inhibition ◽

The Brain ◽

Plasmodial Infection ◽

Stimulation Of

AbstractThe present study aimed to evaluate the effects of dexamethasone on the redox status, parasitemia evolution, and survival rate of Plasmodium berghei-infected mice. Two-hundred and twenty-five mice were infected with Plasmodium berghei and subjected to stimulation or inhibition of NO synthesis. The stimulation of NO synthesis was performed through the administration of L-arginine, while its inhibition was made by the administration of dexamethasone. Inducible NO synthase (iNOS) inhibition by dexamethasone promoted an increase in the survival rate of P. berghei-infected mice, and the data suggested the participation of oxidative stress in the brain as a result of plasmodial infection, as well as the inhibition of brain NO synthesis, which promoted the survival rate of almost 90% of the animals until the 15th day of infection, with possible direct interference of ischemia and reperfusion syndrome, as seen by increased levels of uric acid. Inhibition of brain iNOS by dexamethasone caused a decrease in parasitemia and increased the survival rate of infected animals, suggesting that NO synthesis may stimulate a series of compensatory redox effects that, if overstimulated, may be responsible for the onset of severe forms of malaria.

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Curcumin Potentiates α7 Nicotinic Acetylcholine Receptors and Alleviates Autistic-Like Social Deficits and Brain Oxidative Stress Status in Mice

International Journal of Molecular Sciences ◽

10.3390/ijms22147251 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7251

Author(s):

Petrilla Jayaprakash ◽

Dmytro Isaev ◽

Waheed Shabbir ◽

Dietrich E. Lorke ◽

Bassem Sadek ◽

...

Keyword(s):

Oxidative Stress ◽

Nicotinic Acetylcholine Receptors ◽

Acetylcholine Receptors ◽

Pathological Condition ◽

Repetitive Behaviors ◽

Social Deficits ◽

Nicotinic Acetylcholine ◽

Oxidative Stress Status ◽

Inward Currents ◽

Α7 Nachrs

Autistic spectrum disorder (ASD) refers to a group of neurodevelopmental disorders characterized by impaired social interaction and cognitive deficit, restricted repetitive behaviors, altered immune responses, and imbalanced oxidative stress status. In recent years, there has been a growing interest in studying the role of nicotinic acetylcholine receptors (nAChRs), specifically α7-nAChRs, in the CNS. Influence of agonists for α7-nAChRs on the cognitive behavior, learning, and memory formation has been demonstrated in neuro-pathological condition such as ASD and attention-deficit hyperactivity disorder (ADHD). Curcumin (CUR), the active compound of the spice turmeric, has been shown to act as a positive allosteric modulator of α7-nAChRs. Here we hypothesize that CUR, acting through α7-nAChRs, influences the neuropathology of ASD. In patch clamp studies, fast inward currents activated by choline, a selective agonist of α7-nAChRs, were significantly potentiated by CUR. Moreover, choline induced enhancement of spontaneous inhibitory postsynaptic currents was markedly increased in the presence of CUR. Furthermore, CUR (25, 50, and 100 mg/kg, i.p.) ameliorated dose-dependent social deficits without affecting locomotor activity or anxiety-like behaviors of tested male Black and Tan BRachyury (BTBR) mice. In addition, CUR (50 and 100 mg/kg, i.p.) mitigated oxidative stress status by restoring the decreased levels of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus and the cerebellum of treated mice. Collectively, the observed results indicate that CUR potentiates α7-nAChRs in native central nervous system neurons, mitigates disturbed oxidative stress, and alleviates ASD-like features in BTBR mice used as an idiopathic rodent model of ASD, and may represent a promising novel pharmacological strategy for ASD treatment.

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Nutraceutical Supplementation Ameliorates Visual Function, Retinal Degeneration, and Redox Status in rd10 Mice

Antioxidants ◽

10.3390/antiox10071033 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1033

Author(s):

Lorena Olivares-González ◽

Sheyla Velasco ◽

Isabel Campillo ◽

David Salom ◽

Emilio González-García ◽

...

Keyword(s):

Oxidative Stress ◽

Retinal Degeneration ◽

Antioxidant Properties ◽

Photoreceptor Cells ◽

Redox Status ◽

Inherited Retinal Dystrophies ◽

Stress Markers ◽

Retinal Dystrophies ◽

Progressive Degeneration ◽

Light Stimuli

Background: Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies characterized by progressive degeneration of photoreceptor cells. Ocular redox status is altered in RP suggesting oxidative stress could contribute to their progression. In this study, we investigated the effect of a mixture of nutraceuticals with antioxidant properties (NUT) on retinal degeneration in rd10 mice, a model of RP. Methods: NUT was orally administered to rd10 mice from postnatal day (PD) 9 to PD18. At PD18 retinal function and morphology were examined by electroretinography (ERG) and histology including TUNEL assay, immunolabeling of microglia, Müller cells, and poly ADP ribose polymers. Retinal redox status was determined by measuring the activity of antioxidant enzymes and some oxidative stress markers. Gene expression of the cytokines IL-6, TNFα, and IL-1β was assessed by real-time PCR. Results: NUT treatment delayed the loss of photoreceptors in rd10 mice partially preserving their electrical responses to light stimuli. Moreover, it ameliorated redox status and reduced inflammation including microglia activation, upregulation of cytokines, reactive gliosis, and PARP overactivation. Conclusions: NUT ameliorated retinal functionality and morphology at early stages of RP in rd10 mice. This formulation could be useful as a neuroprotective approach for patients with RP in the future.

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Oxidative Stress as a Possible Target in the Treatment of Toxoplasmosis: Perspectives and Ambiguities

International Journal of Molecular Sciences ◽

10.3390/ijms22115705 ◽

2021 ◽

Vol 22 (11) ◽

pp. 5705

Author(s):

Karolina Szewczyk-Golec ◽

Marta Pawłowska ◽

Roland Wesołowski ◽

Marcin Wróblewski ◽

Celestyna Mila-Kierzenkowska

Keyword(s):

Oxidative Stress ◽

Animal Studies ◽

Treatment Options ◽

Natural Antioxidants ◽

Redox Status ◽

Host Cells ◽

Common Disease ◽

Parasite Viability

Toxoplasma gondii is an apicomplexan parasite causing toxoplasmosis, a common disease, which is most typically asymptomatic. However, toxoplasmosis can be severe and even fatal in immunocompromised patients and fetuses. Available treatment options are limited, so there is a strong impetus to develop novel therapeutics. This review focuses on the role of oxidative stress in the pathophysiology and treatment of T. gondii infection. Chemical compounds that modify redox status can reduce the parasite viability and thus be potential anti-Toxoplasma drugs. On the other hand, oxidative stress caused by the activation of the inflammatory response may have some deleterious consequences in host cells. In this respect, the potential use of natural antioxidants is worth considering, including melatonin and some vitamins, as possible novel anti-Toxoplasma therapeutics. Results of in vitro and animal studies are promising. However, supplementation with some antioxidants was found to promote the increase in parasitemia, and the disease was then characterized by a milder course. Undoubtedly, research in this area may have a significant impact on the future prospects of toxoplasmosis therapy.

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Imaging NAD(H) Redox Alterations in Cryopreserved Alveolar Macrophages from Ozone-Exposed Mice and the Impact of Nutrient Starvation during Long Lag Times

Antioxidants ◽

10.3390/antiox10050767 ◽

2021 ◽

Vol 10 (5) ◽

pp. 767

Author(s):

He N. Xu ◽

Joanna Floros ◽

Lin Z. Li ◽

Shaili Amatya

Keyword(s):

Oxidative Stress ◽

Alveolar Macrophages ◽

Redox State ◽

Redox Status ◽

Nutrient Starvation ◽

Ozone Exposure ◽

Reduced Form ◽

Time Period ◽

Lag Times ◽

The Impact

Employing the optical redox imaging technique, we previously identified a significant redox shift of nicotinamide adenine dinucleotide (NAD and the reduced form NADH) in freshly isolated alveolar macrophages (AM) from ozone-exposed mice. The goal here was twofold: (a) to determine the NAD(H) redox shift in cryopreserved AM isolated from ozone-exposed mice and (b) to investigate whether there is a difference in the redox status between cryopreserved and freshly isolated AM. We found: (i) AM from ozone-exposed mice were in a more oxidized redox state compared to that from filtered air (FA)-exposed mice, consistent with the results obtained from freshly isolated mouse AM; (ii) under FA exposure, there was no significant NAD(H) redox difference between fresh AM that had been placed on ice for 2.5 h and cryopreserved AM; however, under ozone exposure, fresh AM were more oxidized than cryopreserved AM; (iii) via the use of nutrient starvation and replenishment and H2O2-induced oxidative stress of an AM cell line, we showed that this redox difference between cryopreserved and freshly isolated AM is likely the result of the double “hit”, i.e., the ozone-induced oxidative stress plus nutrient starvation that prevented freshly isolated AM from a full recovery after being on ice for a prolonged time period. The cryopreservation technique we developed eliminates/minimizes the effects of oxidative stress and nutrient starvation on cells. This method can be adopted to preserve lung macrophages from animal models or clinical patients for further investigations.

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Fighting Oxidative Stress with Sulfur: Hydrogen Sulfide in the Renal and Cardiovascular Systems

Antioxidants ◽

10.3390/antiox10030373 ◽

2021 ◽

Vol 10 (3) ◽

pp. 373

Author(s):

Joshua J. Scammahorn ◽

Isabel T. N. Nguyen ◽

Eelke M. Bos ◽

Harry Van Goor ◽

Jaap A. Joles

Keyword(s):

Oxidative Stress ◽

Hydrogen Sulfide ◽

Redox Status ◽

The Body ◽

Therapeutic Interventions ◽

Oxygen Species ◽

Enzymatic Production ◽

Age Related ◽

Anti Oxidant ◽

Enzymatic Pathways

Hydrogen sulfide (H2S) is an essential gaseous signaling molecule. Research on its role in physiological and pathophysiological processes has greatly expanded. Endogenous enzymatic production through the transsulfuration and cysteine catabolism pathways can occur in the kidneys and blood vessels. Furthermore, non-enzymatic pathways are present throughout the body. In the renal and cardiovascular system, H2S plays an important role in maintaining the redox status at safe levels by promoting scavenging of reactive oxygen species (ROS). H2S also modifies cysteine residues on key signaling molecules such as keap1/Nrf2, NFκB, and HIF-1α, thereby promoting anti-oxidant mechanisms. Depletion of H2S is implicated in many age-related and cardiorenal diseases, all having oxidative stress as a major contributor. Current research suggests potential for H2S-based therapies, however, therapeutic interventions have been limited to studies in animal models. Beyond H2S use as direct treatment, it could improve procedures such as transplantation, stem cell therapy, and the safety and efficacy of drugs including NSAIDs and ACE inhibitors. All in all, H2S is a prime subject for further research with potential for clinical use.

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