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opencc-zeroApr 2020View details →

Strong species differences in life-history do not predict oxidative stress physiology or sensitivity to an environmental oxidant

1. Species typically align along a fast-slow life-history continuum, yet it is not clear to what extent oxidative stress physiology can be integrated with this continuum to form a 'pace-of-life syndrome', especially so in invertebrates. This is important, given the assumed role of oxidative stress in mediating life-history trade-offs, and the prediction that species with a faster pace should be more vulnerable to oxidative stress. 2. We tested whether a species' life-history pace, here represented by its growth rate, can predict species-level differentiation in physiology and sensitivity to oxidative stress. Therefore, we exposed four species of Ischnura damselflies that strongly align along a fast-slow life-history continuum to different levels of ultraviolet (UV) radiation. We measured an extended set of physiological traits linked to the pace-of-life: standard metabolic rate (SMR), oxidative stress physiology (antioxidant enzymes and oxidative damage), and defence/condition traits (investment in immune function, energy storage, and structural defence). 3. Despite strong species differences in growth rate and physiology, growth rate did not predict species-level differentiation in physiology. Hence there was no support for the integration of metabolic rate, oxidative stress physiology or defence/condition traits into a species-level syndrome. 4. UV exposure affected nearly all traits: it reduced growth rate and increased metabolic rate, affected all oxidative stress physiology traits and increased the two defence traits (immune function, and melanin content). Nevertheless, the pace-of-life based on growth rate did not predict sensitivity to UV. Instead, the observed pattern of investment in structural UV defence (melanin) might have reduced the need for enzymatic antioxidant defence, this way potentially decoupling the covariation between the life-history pace and oxidative stress physiology. 5. The absence of an integrated axis of life-history and physiological variation indicates no major constraints for the evolution of these traits among the studied damselfly species. Our study highlights that ecological differences between species may decouple covariation between species' life-history pace and their physiology, as well as their sensitivity to environmental stressors. 30-Mar-2020

opencc-by-4.0Aug 2017View details →

ROS-specific Huntingtin Interactions: Oxidative Stress Optimization H2O2

Optimization step in the lead up to mass spec identification of ROS-specific huntingtin protein-protein interactions.

opencc-zeroJan 2024View details →

Data from: anterior pituitary transcriptomics following a high fat diet: impact of oxidative stress on cell metabolism

Anterior pituitary cells are highly active with regards to protein synthesis and secretion, processes which depend heavily on mitochondrial ATP production and functional endoplasmic reticula. It is well known that obesity adds an allostatic overload to tissues, requiring them to adapt to inflammation and oxidative stress. Therefore, we hypothesized that the pituitary is highly vulnerable to the stress of high fat diet-induced weight gain. In this study, we utilized a 10-15 week high fat diet (HFD, 60%) plus a thermoneutral housing paradigm, testing both male and female FVB.129P mice. We quantified serum hormones and cytokines, characterized the metabolic phenotype, and defined changes in the pituitary transcriptome using single-cell RNA-seq. Weight gain was significant by 3 weeks in HFD mice, and by 10 weeks all HFD groups had gained 20 g. HFD females (15 weeks) had increased energy expenditure and decreased activity. All HFD groups showed increases in serum leptin, Il-6, resistin, MCP-1, and TNFα. HFD males had increased insulin; both HFD males and females had increased TSH, and HFD females had decreased serum prolactin and growth hormone (GH) pulse amplitude. Pituitary scRNA-seq revealed modest or no changes in pituitary cell gene expression in the different cell types from HFD males after 10 or 15 weeks or HFD females after 10 weeks. However, females exposed to a HFD for 15 weeks showed significant numbers of differentially expressed genes in lactotropes and stem cells. Pathway analyses identified a reduction in pathways that supported protein translation, ribosome biogenesis, and oxidative phosphorylation, indicating mitochondrial dysfunction. Collectively, these studies reveal that pituitary cells from males are more resilient to the oxidative stress of obesity than females and identify the most vulnerable pituitary cell populations in females.

opencc-by-4.0Oct 2024View details →

Mitochondrial oxidant stress promotes alpha-synuclein aggregation and spreading in mice with mutated glucocerebrosidase

These are the data sets and plasmid sequences of the viral vectors used in the study "Mitochondrial oxidant stress promotes alpha-synuclein aggregation and spreading in mice with mutated glucocerebrosidase"

opencc-by-4.0Mar 2022View details →

Role of Alkylhydroperoxidase Rv2159c in the Oxidative Stress Response and Virulence of Mycobacterium tuberculosis

Mycobacterium tuberculosis, which causes tuberculosis, is one of the leading infectious agents worldwide with a high rate of mortality. Following aerosol inhalation, M. tuberculosis primarily infects the alveolar macrophages, which results in a host immune response that gradually activates various antimicrobial mechanisms, including the production of reactive oxygen species (ROS), within the phagocytes to neutralize the bacteria. OxyR is the master regulator of oxidative stress response in several bacterial species. However, due to the absence of a functional oxyR locus in M. tuberculosis, the peroxidase stress is controlled by alkylhydroperoxidases. M. tuberculosis expresses alkylhydroperoxide reductase to counteract the toxic effects of ROS. In the current study, we report the functional characterization of an ortholgue of alkylhydroperoxidase family member, Rv2159c, a conserved protein with putative peroxidase activity, during stress response and virulence of M. tuberculosis. We generated a gene knockout mutant of M. tuberculosis Rv2159c (MtbΔ2159) by specialized transduction. The MtbΔ2159 was sensitive to oxidative stress and exposure to toxic transition metals. In a human monocyte (THP-1) cell infection model, MtbΔ2159 showed reduced intracellular survival and increased expression of pro-inflammatory molecules, includingIL-1β, IP-10 and MIP-1α, compared to the wild type M. tuberculosis and Rv2159c-complemented MtbΔ2159 strains. Similarly, in a guinea pig model of pulmonary infection, MtbΔ2159 displayed growth attenuation in the lungs, compared to the wild type M. tuberculosis and Rv2159c-complemented MtbΔ2159 strains. Our study suggests that Rv2159c has a significant role in maintaining the cellular homeostasis during stress and virulence of M. tuberculosis.

opencc-zeroApr 2022View details →

Astaxanthin from Haematococcus pluvialis prevents high-fat diet-induced hepatic steatosis and oxidative stress in mice by gut-liver axis modulating properties

Scope: Evidence is mounting that astaxanthin (ATX), a xanthophyll carotenoid, used as a nutritional supplement to prevent chronic metabolic diseases. The present study aims to identify the potential function of ATX supplementation in preventing steatohepatitis and hepatic oxidative stress in diet-induced obese mice. Methods and Results: In this study, ATX as dose of 0.25%, 0.5% and 0.75% have orally administered to mice along with a high-fat diet (HFD) to investigate the role of ATX in regulating liver lipid metabolism and gut microbiota. The study showed that ATX dose-dependently reduces body weight, lipid droplet formation, hepatic triglycerides and ameliorated hepatic steatosis and oxidative stress. 0.75% ATX altered the levels of 34 lipid metabolites related to hepatic cholesterol and fatty acid metabolism which might be associated with downregulation of lipogenesis-related genes and upregulation of bile acid biosynthesis-related genes. The result also revealed that ATX alleviates HFD-induced gut microbiota dysbiosis by significantly inhibiting the growth of obesity-related Parabacteroides and Desulfovibrio while promoting the growth of Allobaculum and Akkermansia. Conclusion: The study results suggested that dietary ATX may prevent the development of hepatic steatosis and oxidative stress with the risk of metabolic disease by gut-liver axis modulating properties.

opencc-by-4.0Jun 2023View details →

Figure 1 in Short-time salinity fluctuations are strong activators of oxidative stress in Mediterranean mussel (Mytilus galloprovincialis)

Figure 1. Scheme illustrating the experimental design.

opencc-zeroJul 2023View details →

Evaluation of oxidative stress markers in Rwanda during the SARS-CoV-2 pandemic: a cross-sectional study

SARS-CoV-2 is mainly described as endothelial dysfunction, and due to the bidirectional link between oxidative stress and endothelial dysfunction, we initiated a program directed to the evaluation of the oxidative status of the population of Rwanda by measuring spectrophotometrically their plasma Reactive Oxygen Metabolites (dROMs) and Plasma Antioxidant Potential (PAT). The reference population was chosen to reflect the absence of actual or past SARS-CoV-2 infections as well as other clinically established infective status and reference intervals for d-ROM and PAT were identified. The average d-ROM was 378.6 UCARR with a standard deviation of 105.2. The average PAT value was 2853.6, with a standard deviation of 635.7 UCOR. On the basis of the published values for the Caucasian and East Asian populations, the average value of d-ROM obtained in Rwanda was significantly higher than expected. Conversely, the average PAT value was at the upper limit according to the averaged values for healthy Caucasian populations. The results of this study, the first so far reported on a sub-Saharan population, can effectively be used as a baseline value for clinical management of inflammatory conditions, for the stratification of at-risk individuals and to inform recommendations for effective use of public health resources.

opencc-by-sa-4.0Aug 2023View details →

Dataset on biomarkers for the project "Intermittent hypoxia differentially affects metabolic and oxidative stress responses in two species of cyprinid fish"

The file contains the data for the tissue-level biomarkers evaluating the impact of short-term hypoxia on oxidative stress and metabolic parameters in silver carp Hypophthalmichthys molitrix and gibel carp Carassius gibelio.

opencc-zeroAug 2023View details →

Data from: The CST complex facilitates cell survival under oxidative genotoxic stress

Genomic DNA is constantly exposed to a variety of genotoxic stresses, and it is crucial for organisms to be equipped with mechanisms for repairing the damaged genome. Previously, it was demonstrated that the mammalian CST (CTC1-STN1-TEN1) complex, which was originally identified as a single-stranded DNA-binding trimeric protein complex essential for telomere maintenance, is required for survival in response to hydroxyurea (HU), which induces DNA replication fork stalling. It is still unclear, however, how the CST complex is involved in the repair of diverse types of DNA damage induced by oxidizing agents such as H2O2. STN1 knockdown (KD) sensitized HeLa cells to high doses of H2O2. While H2O2-induced DNA strand breaks throughout the cell cycle, STN1 KD cells were as resistant as control cells to H2O2 treatment when challenged in the G1 phase of the cell cycle, but they were sensitive when exposed to H2O2 in S/G2/M phase. STN1 KD cells showed a failure of DNA synthesis and RAD51 foci formation upon H2O2 treatment. Chemical inhibition of RAD51 in shSTN1 cells did not exacerbate the sensitivity to H2O2, implying that the CST complex and RAD51 act in the same pathway. Collectively, our results suggest that the CST complex is required for maintaining genomic stability in response to oxidative DNA damage, possibly through RAD51-dependent DNA repair/protection mechanisms.

Association Between Increased Oxidative Stress, Anti-Inflammatory Fatty Acid Formation, and Airway Infection in People With Asthma and Chronic Obstructive Pulmonary Disease

ClinicalTrials.gov study NCT00595114. IPD Sharing: Not stated. Countries: 1. Publications: 1.

Oxidative Stress in Women Treated With Atosiban for Impending Preterm Birth

ClinicalTrials.gov study NCT03570294. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.

Effect of Statins on Oxidative Stress and Endothelial Progenitor Cells

ClinicalTrials.gov study NCT00166036. IPD Sharing: Not stated. Countries: 1. Publications: 1.

Effects of Nicotinamide Riboside on Bioenergetics and Oxidative Stress in Mild Cognitive Impairment/Alzheimer's Dementia

ClinicalTrials.gov study NCT04430517. IPD Sharing: YES. Countries: 1. Publications: 0.

closedIPD-NOFeb 2026View details →

Determination of RNA/DNA Damage Associated With Oxidative Stress in Periodontitis Patients

ClinicalTrials.gov study NCT07279896. IPD Sharing: NO. Countries: 1. Publications: 3.

Study of Inflammation and Oxidative Stress in Persons Undergoing Dialysis

ClinicalTrials.gov study NCT00732069. IPD Sharing: Not stated. Countries: 1. Publications: 2.

closedIPD-NOFeb 2026View details →

Oxidative Stress and Surgical Recovery

ClinicalTrials.gov study NCT04732000. IPD Sharing: NO. Countries: 1. Publications: 11.

The Effect of Methylphenidate Treatment on Oxidative Stress Levels in Children Diagnosed With Attention Deficit Hyperactivity Disorder (ADHD)

ClinicalTrials.gov study NCT06844812. IPD Sharing: YES. Countries: 1. Publications: 6.

Effect of Lidocaine-Dexmedetomidine on Pain, Inflammation, and Oxidative Stress After Bariatric Surgery.

ClinicalTrials.gov study NCT07073846. IPD Sharing: YES. Countries: 1. Publications: 30.

"Residual Kidney Function and Oxidative Stress in Incremental vs Standard Peritoneal Dialysis (2 Mexican Centers)"

ClinicalTrials.gov study NCT07338435. IPD Sharing: YES. Countries: 1. Publications: 3.