Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
118
datasets available to search
ShareScore release 0.9.0
Dataset results
118 results for “oxidative damage”
Figure 1 in DNA damage, oxidative stress, decreased viability and motility in common carp (Cyprinuscarpio L.) spermatozoa induced by tryptophan, phenylalanine and cysteine amino acids during short-term storage
Figure 1. Effect of tryptophan (T), phenylalanine (P), cysteine (C) at concentrations of 1, 5, 25, and 50 mM on DNA fragmentation of common carp (Cyprinuscarpio L.) spermatozoa at 6 (a), 24 (b), and 48 (c) h.
Data from: Attractive male sticklebacks carry more oxidative DNA damage in the soma and germline
<p>Trade-offs between the expression of sexual signals and the maintenance of somatic and germline tissues are expected when these depend upon the same resources. Despite the importance of sperm DNA integrity, its trade-off with sexual signalling has rarely been explored. We experimentally tested the trade-off between carotenoid-based sexual colouration and oxidative DNA damage in skeletal muscle, testis and sperm by manipulating reproductive schedule (early <i>vs.</i> late onset of breeding) in male three-spined sticklebacks. Oxidative DNA damage was measured as the amount of 8-hydroxy-2-deoxy-Guanosine in genomic DNA. Irrespective of the experimentally manipulated reproductive schedule, individuals investing more in red colouration showed higher levels of oxidative DNA damage in muscle, testis and sperm during the peak breeding season. Our results show that the expression of red colouration traded off against the level of oxidative DNA damage possibly due to the competing functions of carotenoids as colorants and antioxidants. Thus, female sticklebacks may risk fertility and viability of offspring by choosing redder, more deteriorated partners with decreased sperm DNA integrity. The evolution of sexual signal may be constrained by oxidative DNA damage in the soma and germline. </p>
Data from: Enzyme polymorphism, oxygen and injury: a lipidomic analysis of flight-induced oxidative damage in a SDH-polymorphic insect
When active tissues receive insufficient oxygen to meet metabolic demand, succinate accumulates and has two fundamental effects: it causes ischemia-reperfusion injury while also activating the hypoxia-inducible factor pathway (HIF). The Glanville fritillary butterfly (Melitaea cinxia) possesses a balanced polymorphism in Sdhd, shown previously to affect HIF pathway activation and tracheal morphology and used here to experimentally test the hypothesis that variation in succinate dehydrogenase affects oxidative injury. We stimulated butterflies to fly continuously in a respirometer (3 min duration), which typically caused episodes of exhaustion and recovery, suggesting a potential for cellular injury from hypoxia and reoxygenation in flight muscles. Indeed, flight muscle from butterflies flown on consecutive days had lipidomic profiles similar to rested paraquat-injected butterflies, but distinct from rested untreated butterflies. Many butterflies showed a decline in flight metabolic rate (FMR) on Day 2, and there was a strong inverse relationship between the ratio of Day 2 to Day 1 FMR and the abundance of sodiated adducts of phosphatidylcholines and coenzyme Q (CoQ). This result is consistent with elevation of sodiated lipids caused by disrupted intracellular ion homeostasis in mammalian tissues after hypoxia-reperfusion. Butterflies carrying the Sdhd M allele had higher abundance of lipid markers of cellular damage, but the association was reversed in field-collected butterflies, where focal individuals typically flew for seconds at a time rather than continuously. These results indicate that Glanville fritillary flight muscles can be injured by episodes of high exertion, but injury severity appears to be determined by an interaction between SDH genotype and behavior (prolonged vs. intermittent flight).
Raw data of Octopus maya embryos along the development: wet weight, oxygen consumption, antioxidant defence mechanisms and oxidative damage.
<p>Raw data on oxygen consumption and antioxidant defense mechanisms of Octopus maya embryos were maintained in laboratory conditions at 24°C. Those data were obtained during the embryo development. The antioxidant defense mechanisms and oxidant damage were also obtained from the ovary and the un-spawned eggs, allowing to us known how is the oxidant damage translated from the females to embryos in this octopus species. </p>
CO2 Protects Cells from Iron-Fenton Oxidative DNA Damage in E. coli and Humans
<p>Whereas hydroxyl radical is commonly named as the Fenton product responsible for DNA and RNA<br>damage in cells, here we demonstrate that the cellular reaction generates carbonate radical<br>anion due to physiological levels of bicarbonate. Analysis of the metabolome, the transcriptome,<br>and the human genome shows a consistent buffering of H2O2-induced oxidative<br>stress leading to one common pathway, namely guanine oxidation. Particularly revealing are nanopore-<br>based studies of direct RNA sequencing of cytosolic and mitochondrial ribosomal RNA along with<br>glycosylase-dependent qPCR studies of oxidative DNA damage in telomeres. The focusing of oxidative<br>modification on one pathway is consistent with the highly evolved base excision repair suite of enzymes<br>and their involvement in gene regulation in response to oxidative stress.</p>
Determination of RNA/DNA Damage Associated With Oxidative Stress in Periodontitis Patients
ClinicalTrials.gov study NCT07279896. IPD Sharing: NO. Countries: 1. Publications: 3.
The Effect of Protandim Supplementation on Oxidative Damage and Athletic Performance
ClinicalTrials.gov study NCT02172625. IPD Sharing: YES. Countries: 1. Publications: 7.
An Eval of Neurocognitive Function, Oxidative Damage, and Their Association With Outcomes in METH and Cocaine Abusers.
ClinicalTrials.gov study NCT00628927. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Data from: Attractive male sticklebacks carry more oxidative DNA damage in the soma and germline
Open the record for dataset details and reuse information.
Data from: DNA damage signaling in Drosophila macrophages modulates systemic cytokine levels in response to oxidative stress
Open the record for dataset details and reuse information.
Data from: Flying stimulates the antioxidant system and protects against oxidative damage in a migratory songbird, yet diet quality has little effect
Open the record for dataset details and reuse information.
Data from: Micronuclear collapse from oxidative damage
Open the record for dataset details and reuse information.
Data from: Enzyme polymorphism, oxygen and injury: a lipidomic analysis of flight-induced oxidative damage in a SDH-polymorphic insect
Open the record for dataset details and reuse information.
Data from: Oxidative damage to lipids is rapidly reduced during migratory stopovers
Open the record for dataset details and reuse information.
Data from: Oxidative damage and antioxidant defence are assay and tissue dependent both in captive and in wild-caught bank voles (Myodes glareolus) before and after reproduction
1. Reproduction is costly and life-history theory predicts that current parental investment will result in lower survival or decreased future reproduction. The physiological mechanisms mediating the link between reproduction and survival are still under debate and elevated oxidative damage during reproduction has been proposed as a plausible candidate. 2. Previous studies of oxidative stress during reproduction in animals under natural conditions have been restricted to analyses of blood. Herein, we measured the level of oxidative damage to lipids (thiobarbituric-acid-reactive substances) and proteins (carbonyls) in the liver, kidneys, heart and skeletal muscles in free-living bank vole females from spring and autumn generations, before and after reproduction. Antioxidant defence in the liver and kidneys was also determined. We expected oxidative damage to tissues and hypothesized that the damage would be more uniform between tissues in wild animals compared to those breeding under laboratory conditions. 3. Considering all combinations of markers/tissues/generations, oxidative damage in females did not differ before and after reproduction in 12 comparisons, was lower after reproduction in 3 comparisons, and was higher after breeding in one comparison. The total glutathione was significantly increased after reproduction only in the liver of the autumn generation and there was no change in catalase activity. 4. Our results confirm – for the first time in the field – previous observations from laboratory studies that there is no simple link between oxidative stress and reproduction and that patterns depend on the tissue and marker being studied. Overall however, our study does not support the hypothesis that the cost of reproduction in bank voles is mediated by oxidative stress in these tissues.
Neutrophil-mediated oxidative stress and albumin structural damage predict COVID-19-associated mortality
<p>This work reports that COVID-19-induced oxidative stress inflicts structural damages to human serum albumin (HSA) and is linked with mortality outcome in critically ill patients. Analyzing blood samples from patients and healthy individuals, the paper provides evidence that neutrophils are major sources of oxidative stress in blood and that hydrogen peroxide is highly accumulated in plasmas of non-survivors. The electron paramagnetic resonance spectra of spin-labeled fatty acids (SLFAs) bound with HSA in whole blood of control, survivor, and non-survivor subjects (n=10–11) were analyzed to probe structural damages to the protein. Non-survivors' HSA showed dramatically altered biophysical parameters that reflect remarkably fluid protein microenvironments. Following loading/unloading of 16-DSA, the results show that the transport function of HSA may be impaired in severe patients. Stratified at the means, Kaplan–Meier survival analysis indicated that lower values of S/W ratio and accumulated H<sub>2</sub>O<sub>2</sub> in plasma significantly predicted in-hospital mortality.</p>
Theoretical insights into the antiradical activity and copper-catalyzed oxidative damage of mexidol in the physiological environment
<p>This dataset contains data from the calculations described in the paper: "Quan V. Vo*, Nguyen Thi Hoa, <span class="fontstyle01"><span>Mai Van Bay, </span></span>Adam Mechler, Theoretical insights into the antiradical activity and copper-catalyzed oxidative damage of mexidol in the physiological environment. Royal Society Open Science. 2021.</p> <p>In this study, the hydroperoxyl radical scavenging activity of<b> MD </b>was studied to establish baseline antioxidant activity, followed by an investigation of the effect of<b> MD </b>on the <span class="fontstyle01"><span>copper-catalyzed oxidative damage in</span></span> <span class="fontstyle01"><span>biological systems, using computational methods. It was found that</span></span><span class="fontstyle01"><span><b> MD </b></span></span><span class="fontstyle01"><span>exhibits moderate </span></span>radical scavenging activity against HOO<sup>·</sup> in physiological environments. The activity in aqueous solution is defined by the single electron transfer mechanism of the anion state; however in nonpolar environments the formal hydrogen transfer pathway dominates at the O3-H bond. It was also confirmed that<b> MD </b><span class="fontstyle01"><span>can chelate Cu (II), forming complexes that are much harder to reduce than free Cu (II):</span></span><span class="fontstyle01"><span><b> MD </b></span></span><span class="fontstyle01"><span>chelation completely quenches the Cu (II) reduction by ascorbic acid and suppresses the rate of reduction reaction by O<sub>2</sub></span></span><span class="fontstyle01"><span><sup>·</sup></span></span><span class="fontstyle01"><span><sup>-</sup></span></span><span class="fontstyle01"><span> that are the main reductants of Cu (II) in biological environments. Therefore,</span></span><span class="fontstyle01"><span><b> MD </b></span></span><span class="fontstyle01"><span>exerts its anti- HO</span></span><span class="fontstyle01"><span><sup>·</sup></span></span><span class="fontstyle01"><span><sup> </sup></span></span><span class="fontstyle01"><span>activity primarily as an OIL-1 inhibitor. </span></span></p>
Data from: Inter-generational costs of oxidative stress: reduced fitness in daughters of mothers that experienced high levels of oxidative damage during reproduction
<p>Parental condition transfer effects occur when the parents' physiological state during reproduction affects offspring performance. Oxidative damage may mediate such effects, yet evidence that oxidative damage experienced by parents during reproduction negatively affects offspring fitness is scarce and limited to early life stages. We show in Japanese quail (<em>Coturnix japonica</em>) that maternal levels of oxidative damage, measured during reproduction, negatively predict the number of offspring produced by daughters. This maternal effect on the daughter's reproductive success was mediated by an effect on hatching success, rather than the number of eggs laid by daughters. We also observed a negative association between the father's oxidative damage levels and the number of eggs laid by daughters, but a positive association between the father's oxidative damage levels and the hatching success of these eggs. These opposing paternal effects cancelled each other out, resulting in no overall effect on the number of offspring produced by daughters. No significant association between a female's own level of oxidative damage during reproduction and her reproductive success was observed. Our results suggest that oxidative damage experienced by parents may be a better predictor of an individual's reproductive performance than oxidative damage experienced by the individual itself. Although the mechanisms underlying these parental condition transfer effects are currently unknown, changes in egg composition or (epi-)genetic alterations of gametes may play a role. These findings highlight the importance of an inter-generational perspective when quantifying costs of physiological stress.</p>
Histopathological, Oxidative Stress, and DNA Damage Assessment in the Vas Deferens Tissue of the Freshwater Leech Erpobdella johanssoni (Johansson, 1927) Following BTEX Exposure
Open the record for dataset details and reuse information.
JM-20 administration to animals with lesion of the nigrostriatal dopamine pathway induced by 6-hydroxydopamine, partially reverses motor damage and oxidative stress
<p><strong><span>Abstract</span></strong></p> <p><span>Previous studies have shown that JM-20, a new chemical hybrid molecule, protects against rotenone and 6-hydroxydopamine <span>(6-OHDA)</span> neurotoxicity. Also, we demonstrated that JM-20 blocks the formation of toxic alpha-synuclein aggregated species and <em><span>aminochrome </span></em>cytotoxicity. The present study sought to determine the neuroprotective property of JM-20 in animals with a partial <span>lesion of the nigrostriatal dopamine pathway induced by 6-OHDA </span>. For <em><span>in vivo</span></em> studies, adult male Wistar rats were lesioned in the right <em><span>substantia nigra pars compacta</span></em> (SNpc) upon the administration of 6-OHDA. Fifteen days after surgery, the animal’s asymmetry levels were assessed. Those with asymmetry values higher than 50% were divided into two groups: animals that did not receive any treatment and those that were administered with JM-20 (40 mg/kg, intragastric via gavage) for 27 days. Every seven days, the asymmetry values of the animals were analyzed until day 42 after the surgery. At the end of the experiment, the animals were euthanized and the SNpc and striatum were taken out for the analysis of oxidative stress. Our results reveal a behavioral function progressively recovered in the JM-20-treated animals, diminishing the percentage of motor asymmetry. Also, it ameliorates the oxidative stress in the SNpc and the striatal tissue of these animals. Our study provides the preclinical evidence to support the long term neuroprotective potential of JM-20 in 6-OHDA hemiparkinson's rat model, pointing out to its possible use as a disease-modifying agent in PD.</span></p>
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.