Redox Report最新文献

Objectives: Although glutamate is an essential factor in the neuronal system, excess glutamate can produce excitotoxicity. We previously reported that Peroxiredoxin 5 (Prx5) protects neuronal cells from glutamate toxicity via its antioxidant effects. However, it is unclear whether cytosolic or mitochondrial Prx5 provides greater neuroprotection. Here, we investigated differences in the neuroprotective effects of cytosolic and mitochondrial Prx5.Methods: We analyzed patterns of cytosolic and mitochondrial H₂O₂ generation in glutamate toxicity using HyPer protein. And then, we confirmed the change of intracellular ROS level and apoptosis with respective methods. The mitochondrial dynamics was assessed with confocal microscope imaging and western blotting.Results: We found that the level of mitochondrial H₂O₂ greatly increased compared to cytosolic H₂O₂ and it affected cytosolic H₂O₂ generation after glutamate treatment. In addition, we confirmed that mitochondrial Prx5 provides more effective neuroprotection than cytosolic Prx5.Discussion: Overall, our study reveals the mechanisms of cytosolic and mitochondrial ROS in glutamate toxicity. Our findings suggest that mitochondrial ROS and Prx5 are attractive therapeutic targets and that controlling these factors be useful for the prevention of neurodegenerative diseases.

Background: COVID-19 is characterized by the presence of oxidative stress. Vitamin D status has been reviewed as one of the factors that may affect disease severity. The aim of this study was to assess the relationship between serum vitamin D levels, oxidative stress markers and disease severity in hospitalized COVID-19 patients.

Methods: Vitamin D levels were measured in 33 patients with COVID-19. The total antioxidant power and plasma peroxides were determined in serum.

Results: Severe COVID-19 patients have lower vitamin D levels (18.39 ± 2.29 ng/mL vs. 28.47 ± 3.05 ng/mL, p < .05) and higher oxidative stress compared to the moderate group. When divided according to serum vitamin D levels, significantly higher values of LDH (604.8 ± 76.98 IU/mL vs. 261.57 ± 47.33 IU/mL) and D-dimer (5978 ± 2028ng/mL vs. 977.7 ± 172 ng/mL) were obtained in the group with vitamin D below 30 ng/mL, followed with significantly higher levels of plasma peroxides (d-ROMs: 414.9 ± 15.82 U.Carr vs. 352.4 ± 18.77 U.Carr; p < .05) and oxidative stress index (OSI: 92.25 ± 6.60 vs. 51.89 ± 6.45; p < .001).

Conclusion: The presented data provide a justification to consider vitamin D as an important factor that could ameliorate disease severity through its anti-inflammatory and antioxidant effects.

Objectives: The beneficial role of ROS was probably in promoting intercellular communication by modifying membrane constituents [Liang D. A salutary role of reactive oxygen species in intercellular tunnel-mediated communication. Front Cell Dev Biol. 2018;6:2]. We investigated how the membrane lipids were responding to ROS and ROS inhibitors.Methods: To examine how ROS affected the lipid profiles, we used thin-layer chromatography to characterize lipid profiles in Arabidopsis plants. Then, the confocal microscopy imaging was used to confirm the change of membrane lipid in a plasma membrane marker line exposed to ROS and ROS inhibitors.Results: We found the relative contents of most lipids in H₂O₂-treated Arabidopsis plants were increased in roots, rather than in shoots. The increased fluorescent signal of membrane marker induced by H₂O₂ was mainly enriched in the conductive parts of roots. Several ROS inhibitors also strongly affected the lipid profiles. Among them, diethyldithiocarbamate (DDC) can progressively change the lipid profiles with treatment going on. Membrane marker signal was mainly accumulated in the root tips and epidermal cells after treatment by DDC.Discussion: H₂O₂ may enhance intercellular communication by inducing different lipid species in the conductive parts of roots. The lipid profiles were widely responding to various ROS reagents and might play a role in intercellular signaling.

Objectives: Nitric oxide (NO) plays a vital role in neurological development. As an easily accessible and non-invasive fluid, saliva hasn't been evaluated for nitrite among children with autism spectrum disorder (ASD). This study aims to quantify saliva nitrite and explore its relation with serum NO.

Methods: Saliva sampling and pretreatment methods were optimized, followed by NO measurement via chemiluminescence for 126 ASD children and 129 normally developing children (ND).

Results: In the ASD group, saliva nitrite was significantly higher than that in the ND, with concentrations of 4.97 ± 3.77 μM and 2.66 ± 2.07 μM (p < 0.0001), respectively. Positive correlation was observed between saliva NO₂^- and serum NO₃^- in ASD children, which didn't exist in the ND group. Male children in the ASD group had significantly higher NO than that in boys of the ND group, without significant difference between girls in both groups. Correlation was not found between saliva or serum NO and severity of these ASD children.

Discussion: It is reported for the first time that saliva nitrite was positively correlated with serum nitrate in ASD children, with significantly higher NO only in autistic boys. Non-invasive saliva might serve as a predictor of health status of ASD children.

Objectives: The study explores the protective role of the peripheral serum of limb remote ischemic postconditioning (LRIP) in reducing the reactive oxygen species (ROS) levels and neutrophil activation, which are responsible for the deleterious reperfusion injury.

Methods: LRIP was induced in Sprague-Dawley rats by three cycles of 5 min occlusion /5 min reperfusion on the left hind limb. The blood samples were collected before LRIP or 0 and 1 h after LRIP (named Serum_Sham, Serum_LRIP0, Serum_LRIP1, respectively). The effects of LRIP serum on ROS level and neutrophils activation were determined. The expression of MyD88-TRAF6-MAPKs and PI3K/AKT pathways in neutrophils were examined.

Results: When compared with Serum_Sham, Serum_LRIP0 and Serum_LRIP1 significantly reduced the ROS released from neutrophils activated by fMLP. Meanwhile, the mRNA expression levels of NADPH oxidase subunit p22^phox and multiple ROS-producing related key proteins, such as NADPH oxidase subunit p47^phox ser 304, ser 345. MyD88, p-ERK, p-JNK and p-P38 expression of neutrophils were downregulated by Serum_LRIP0 and Serum_LRIP1. Serum_LRIP1 also downregulated p47^phox mRNA expression and tumor necrosis factor receptor-associated factor 6 (TRAF6) protein expression.

Conclusion: LRIP serum protects against ROS level and neutrophils activation involving the MyD88-TRAF6-MAPKs. This finding provides new insight into the understanding of LRIP mechanisms.

Objectives: High dose-rate ionizing radiation (IR) causes severe DSB damage, as well as reactive oxygen species (ROS) accumulation and oxidative stress. However, it is unknown what biological processes are affected by low dose-rate IR; therefore, the molecular relationships between mitochondria changes and oxidative stress in human normal cells was investigated after low dose-rate IR.Methods: We compared several cellular response between high and low dose-rate irradiation using cell survival assay, ROS/RNS assay, immunofluorescence and western blot analysis.Results: Reduced DSB damage and increased levels of ROS, with subsequent oxidative stress responses, were observed in normal cells after low dose-rate IR. Low dose-rate IR caused several mitochondrial changes, including morphology mass, and mitochondrial membrane potential, suggesting that mitochondrial damage was caused. Although damaged mitochondria were removed by mitophagy to stop ROS leakage, the mitophagy-regulatory factor, PINK1, was reduced following low dose-rate IR. Although mitochondrial dynamics (fission/fusion events) are important for the proper mitophagy process, some mitochondrial fusion factors decreased following low dose-rate IR.Discussion: The dysfunction of mitophagy pathway under low dose-rate IR increased ROS and the subsequent activation of the oxidative stress response.

Background: Oxidative stress is the result of cellular troubles related to aerobic metabolism. Furthermore, this stress is always associated with biological responses evoked by physical, chemical, environmental, and psychological factors. Several studies have developed many approaches of antioxidant defense to diminish the severity of many diseases. Ghrelin was originally identified from the rat stomach, and it is a potent growth hormone-releasing peptide that has pleiotropic functions.

Methods: A systematic review was conducted within PubMed, ScienceDirect, MEDLINE, and Scopus databases using keywords such as ghrelin, antioxidant, oxidative stress, and systemic oxidative stress sensor.

Results: In the last decade, many studies show that ghrelin exhibits protection effects against oxidative stress derived probably from its antioxidant effects. Pieces of evidence demonstrate that systemic oxidative stress increase ghrelin levels in the plasma. The expression of ghrelin and its receptor in ghrelin peripheral tissues and extensively in the central nervous system suggests that this endogenous peptide plays an important role as a systemic oxidative stress sensor.

Conclusion: The current evidence confirms that ghrelin and its derived peptides (Desacyl-ghrelin, obestatin) act as a protective antioxidant agent. Therefore, stressor modality, duration, and intensity are the parameters of oxidative stress that must be taken into consideration to determine the role of ghrelin, Desacyl-ghrelin, and obestatin in the regulation of cell death pathways.

Objective: Ginger (Zingiber officinale Roscoe) is considered to be one of the most commonly consumed dietary condiments of the world. The present study was designed to explicate the protective role of zingerone; an active ingredient of ginger in complete Freund's adjuvant (FCA)-immunized arthritic rats.

Methods: 24 Wistar rats were divided into 4 groups with 6 rats each. Group I as control followed by group II, III and IV were treated with single intradermal injection of FCA (0.1 ml = 100 µg) to induce rheumatoid arthritis. Group III and IV were also administered with zingerone orally at 25 mg/kg b.w for 3 weeks at two different time points.

Results: Adjuvant-treated rats exhibited a significant increase in lipid peroxidation and a reduction in the enzymatic antioxidants such as SOD, catalase and GPx, in the liver and joint tissues. Moreover, FCA inoculation resulted in the increase in levels of NF-κB, TGF-β, TNF-α, IL-1β, IL-6 and Hs-CRP and a decrease in IL-10 levels. Zingerone significantly reduced the levels of NF-κB, TGF-β, TNF-α, IL-1β, IL-6 and Hs-CRP and markedly increased IL-10 levels. Levels of antioxidant enzymes were also restored by zingerone treatment.

Discussion: Oral administration of zingerone ameliorated inflammatory outburst and decreased oxidative stress, suggesting its role in the prevention of rheumatoid arthritis. Further mechanistic insights are necessary to study the exact mechanism involved.

Objective: Acute brain ischemia is accompanied by a disruption of low-molecular-weight aminothiols (LMWTs) homeostasis, such as homocysteine (Hcy), cysteine (Cys), and glutathione (GSH). We investigated the redox balance of LMWTs in blood plasma and its influence on ischemic stroke severity and the functional outcome in patients with an acute period.

Patients and methods: A total of 177 patients were examined. Total and reduced forms of LMWTs were determined in the first 10-24 h. Stroke severity and functional state were estimated using the National Institutes of Health Stroke Scale (NIHSS) and the modified Rankin Scale (mRs) at admission and after 21 days.

Results: Patients with high levels of total Hcy (> 19 μM) showed significantly reduced redox statuses of all LMWTs. Patients with low total GSH levels (≤ 1.07 μM) were at an increased risk of higher stroke severity (NIHSS > 10) compared to patients with a total GSH level > 2.64 μM (age/gender-adjusted odds ratio: 4.69, 95% CI: 1.43-15.4).

Discussion: (1) low total GSH level can be considered as a novel risk marker for the severity of acute stroke in conditions of low redox status of LMWTs and (2) high Hcy levels associated with low redox status of LMWTs.

Objectives: The present study was to isolate the biflavonoid (a bimolecular kaemferol structured molecule) and test its efficacy on oxidative stress and carbohydrate metabolic key enzymes in control and high fat diet and streptozotocin -induced diabetic rats.Methods: Type 2 diabetes was induced in male albino wistar rats by feeding them with high fat diet comprising of 84.3% standard laboratory chow, 5% lard, 10% yolk powder, cholesterol 0.2%, and 0.5% bile salt for 2 weeks. After 2 weeks, the animals were kept in an overnight fast and injected with low dose of streptozotocin (35 mg/kg, dissolved in 0.1 M sodium citrate buffer, pH 4.5).Results: At the end of the experimental period, diabetic control rats showed significant increase in plasma glucose, homeostatic model assessment of insulin resistance (HOMA-IR), glycosylated hemoglobin (HbA1c) with concomitant decrease in plasma insulin, total hemoglobin and body weight. The activities of key enzymes of carbohydrate metabolism, lipid peroxidation markers, antioxidant enzymes, glycogen content and glycogen synthase and glycogen phosphorylase were also altered in diabetic rats.Discussion: Oral administration of biflavonoid to diabetic rats significantly ameliorated all the biochemical alterations to near normal levels. The effect produced by the biflavonoid on various parameters was comparable to that of metformin.