Find research datasets worth reusing

opencc-by-4.0Jan 2020View details →

Figure 2 from: Kondeva-Burdina M, Krasteva I, Popov G, Manov V (2019) Neuroprotective and antioxidant activities of saponins' mixture from Astragalus glycyphylloides in a model of 6-hydroxydopamine-induced oxidative stress on isolated rat brain synaptosomes. Pharmacia 66(4): 233-236. https://doi.org/10.3897/pharmacia.66.e37997

Figure 2 Effects of PSM and S on GSH level in conditions of 6-OHDA-induced oxidative stress ***P ≤ 0.001 vs control (non-treated synaptosomes); +P ≤ 0.05, ++P ≤ 0.01 vs6-OHDA.

opencc-by-4.0Nov 2019View details →

Fig. 1. Glutathione-S in Water pH and hardness alter ATPases and oxidative stress in the gills and kidney of pacu (Piaractus mesopotamicus)

Fig. 1. Glutathione-S-transferase (GST) activity (nmol CNDB-GSH min-1 mg wet tissue-1) in a. gills and b. kidney of pacu (Piaractus mesopotamicus) juveniles under different water hardness and pH at different times. LWH = low water hardness (50 mg CaCO L-1); HWH = high water hardness (120 mg CaCO L-1). Data are presented as the means ± SEM (n = 9 fish 3 3 treatment–1). Different uppercase letters indicate statistically significant differences between pH at the same hardness (P <0.05). Different lowercase letters indicate statistically differences between hardness at the same pH (P <0.05).

opencc-by-4.0Mar 2020View details →

Raw data related to: Sample Size for Oxidative Stress and Inflammation When Treating Multiple Sclerosis with Interferon-b1a and Coenzyme Q10

Abstract  Studying multiple sclerosis (MS) and its treatments requires the use of biomarkers for underlying pathological mechanisms. We aim to estimate the required sample size for detecting variations of biomarkers of inflammation and oxidative stress. This is a post-hoc analysis on 60 relapsing-remitting MS patients treated with Interferon-1a and Coenzyme Q10 for 3 months in an open-label crossover design over 6 months. At baseline and at the 3 and 6-month visits, we measured markers of scavenging activity, oxidative damage, and inflammation in the peripheral blood (180 measurements). Variations of laboratory measures (treatment eect) were estimated using mixed-eect linear regression models (including age, gender, disease duration, baseline expanded disability status scale (EDSS), and the duration of Interferon-1a treatment as covariates; creatinine was also included for uric acid analyses), and were used for sample size calculations. Hypothesizing a clinical trial aiming to detect a 70% eect in 3 months (power = 80% alpha-error = 5%), the sample size per treatment arm would be 1 for interleukin (IL)-3 and IL-5, 4 for IL-7 and IL-2R, 6 for IL-13, 14 for IL-6, 22 for IL-8, 23 for IL-4, 25 for activation-normal T cell expressed and secreted (RANTES), 26 for tumor necrosis factor (TNF)-, 27 for IL-1, and 29 for uric acid. Peripheral biomarkers of oxidative stress and inflammation could be used in proof-of-concept studies to quickly screen the mechanisms of action of MS treatments. Progetto giovani ricercatori [GR-2016-02363725] dal titolo: "Immune Tolerance, Metabolism and Multiple Sclerosis: Novel Molecular Tools to Monitor Disease Pathogenesis and Progression"

opencc-by-4.0Mar 2020View details →

Raw data related to: Coenzyme Q10 supplementation reduces peripheral oxidative stress and inflammation in interferon-β1a-treated multiple sclerosis

Abstract Background: Oxidative stress is a driver of multiple sclerosis (MS) pathology. We evaluated the effect of coenzyme Q10 (CoQ10) on laboratory markers of oxidative stress and inflammation, and on MS clinical severity. Methods: We included 60 relapsing–remitting patients with MS treated with interferon beta1a 44μg (IFN-β1a) with CoQ10 for 3 months, and with IFN-β1a 44μg alone for 3 more months (in an open-label crossover design). At baseline and at the 3 and 6-month visits, we measured markers of scavenging activity, oxidative damage and inflammation in the peripheral blood, and collected data on disease severity. Results: After 3 months, CoQ10 supplementation was associated with improved scavenging activity (as mediated by uric acid), reduced intracellular reactive oxygen species production, reduced oxidative DNA damage, and a shift towards a more anti-inflammatory milieu in the peripheral blood [with higher interleukin (IL)-4 and IL-13, and lower eotaxin, granulocyte-macrophage colonystimulating factor (GM-CSF), hepatocyte growth factor (HGF), interferon (IFN)-γ, IL-1α, IL-2R, IL-9, IL-17F, macrophage inflammatory proteins (MIP)-1α, regulated on activation-normal T cell expressed and secreted (RANTES), tumor necrosis factor (TNF)-α, and vascular endothelial growth factor (VEGF). Also, CoQ10 supplementation was associated with lower Expanded Disability Status Scale, fatigue severity scale, Beck’s depression inventory, and the visual analogue scale for pain. Conclusions: CoQ10 supplementation improved scavenging activity, reduced oxidative damage, and induced a shift towards a more anti-inflammatory milieu, in the peripheral blood of relapsing–remitting MS patients treated with 44μg IFN-β1a 44μg. A possible clinical effect was noted but deserves to be confirmed over longer follow ups. Progetto giovani ricercatori [GR-2016-02363725] dal titolo: "Immune Tolerance, Metabolism and Multiple Sclerosis: Novel Molecular Tools to Monitor Disease Pathogenesis and Progression"

opencc-zeroAug 2020View details →

Radical change: Temporal patterns of oxidative stress during social ascent in a dominance hierarchy

Dominant individuals have priority access to mates and resources. However, high rank can be costly too, especially when it is maintained by intense agonistic behavior. Oxidative stress has been proposed as a potential cost of social dominance. However, social dominance hierarchies can be dynamic, and few studies have examined the cost of social dominance when males are changing status. We studied temporal changes in markers of oxidative stress during social ascent in the East African cichlid fish Astatotilapia burtoni. After removing the dominant male, males ascended from subordinate to dominant status. On the first day of social ascent, immediately after the dominant male removal, the newly dominant male showed lower levels of plasma total antioxidant capacity (TAC). However, we found that liver TAC and liver superoxide dismutase, an enzymatic antioxidant, were significantly upregulated on day 1 and 2 of social ascent, respectively. By day 14, all markers of oxidative stress were similar to those observed in stable dominant males, which has higher levels of reactive oxygen metabolites (ROM) compared to subordinate males. We conclude that markers of oxidative stress vary dramatically during social ascent in a time- and tissue-sensitive manner. Our study provides a more nuanced look at the oxidative cost of social dominance and highlights the importance of considering temporal changes in markers of oxidative stress during important life-history events.

opencc-zeroDec 2019View details →

Data from: Oxidative stress experienced during early development influences the offspring phenotype

Oxidative stress (OS) experienced early in life can affect an individual's phenotype. However, its consequences for the next generation remain largely unexplored. We manipulated the OS level endured by zebra finches (Taeniopygia guttata) during their development by transitorily inhibiting the synthesis of the key antioxidant glutathione ('early-high-OS'). The offspring of these birds and control parents were cross-fostered at hatching to enlarge or reduce its brood size. Independently of parents' early-life OS levels, the chicks raised in enlarged broods showed lower erythrocyte glutathione levels, revealing glutathione sensitivity to environmental conditions. Control ("early-low-OS") biological mothers produced females, not males, that attained a higher body mass when raised in a benign environment (i.e. the reduced brood). In contrast, biological mothers exposed to early-life OS produced heavier males, not females, when allocated in reduced broods. Early-life OS also affected the parental rearing capacity because 12d-old nestlings raised by a foster pair with both early-high-OS members grew shorter legs (tarsus) than chicks from other groups. The results indicate that environmental conditions during development can affect early glutathione levels, which may, in turn, influence the next generation through both pre- and postnatal parental effects. The results also demonstrate that early-life OS can constrain the offspring phenotype.

opencc-zeroDec 2015View details →

Data from: Meta-analysis indicates that oxidative stress is both a constraint on and a cost of growth

Oxidative stress (OS) as a proximate mechanism for life-history trade-offs is widespread in the literature. One such resource allocation trade-off involves growth rate, and theory suggests that OS might act as both a constraint on and a cost of growth, yet studies investigating this have produced conflicting results. Here, we use meta-analysis to investigate whether increased OS levels impact on growth (OS as a constraint on growth) and whether greater growth rates can increase OS (OS as a cost of growth). The role of OS as a constraint on growth was supported by the meta-analysis. Greater OS, in terms of either increased damage or reduced levels of antioxidants, was associated with reduced growth although the effect depended on the experimental manipulation used. Our results also support an oxidative cost of growth, at least in terms of increased oxidative damage, although faster growth was not associated with a change in antioxidant levels. These findings that OS can act as a constraint on growth support theoretical links between OS and animal life histories and provide evidence for a growth–self-maintenance trade-off. Furthermore, the apparent oxidative costs of growth imply individuals cannot alter this trade-off when faced with enhanced growth. We offer a starting platform for future research and recommend the use of oxidative damage biomarkers in nonlethal tissue to investigate the growth–OS relationship further.

Data from: Longevity and life history coevolve with oxidative stress in birds

1. The mechanisms that underpin the evolution of ageing and life histories remain elusive. Oxidative stress, which results in accumulated cellular damages, is one of the mechanisms suggested to play a role. 2. In this paper we set out to test the 'oxidative stress theory of ageing' and the 'oxidative stress hypothesis of life histories' using a comprehensive phylogenetic comparison based on an unprecedented dataset of oxidative physiology in 88 free-living bird species. 3. We show for the first time that bird species with longer lifespan have higher non-enzymatic antioxidant capacity and suffer less oxidative damage to their lipids. We also found that bird species featuring a faster pace-of-life either feature lower non-enzymatic antioxidant capacity or are exposed to higher levels of oxidative damage, while adult annual mortality does not relate to oxidative state. 4. These results reinforce the role of oxidative stress in the evolution of lifespan and also corroborate the role of oxidative state in the evolution of life histories among free-living birds.

opencc-zeroDec 2012View details →

Data from: A trade-off between oxidative stress resistance and DNA repair plays a role in the evolution of elevated mutation rates in bacteria

The dominant paradigm for the evolution of mutator alleles in bacterial populations is that they spread by indirect selection for linked beneficial mutations when bacteria are poorly adapted. In this paper, we challenge the ubiquity of this paradigm by demonstrating that a clinically important stressor, hydrogen peroxide, generates direct selection for an elevated mutation rate in the pathogenic bacterium Pseudomonas aeruginosa as a consequence of a trade-off between the fidelity of DNA repair and hydrogen peroxide resistance. We demonstrate that the biochemical mechanism underlying this trade-off in the case of mutS is the elevated secretion of catalase by the mutator strain. Our results provide the first experimental evidence that direct selection can favour mutator alleles in bacterial populations, and pave the way for future studies to understand how mutation and DNA repair are linked to stress responses and how this impacts the evolution of bacterial mutation rates.

Data from: Resveratrol supplementation reduces oxidative stress and modulates the immune response in free-living animals during a viral infection

1. Diet quality may have an important effect on the regulation of oxidative status and the immune system during an infectious disease. However, the relationship among intake of specific dietary molecules, an individual's oxidative status and the occurrence and progress of a viral disease remains almost unexplored in free-living organisms. 2. Here, we study a wild, long-lived animal, the Magnificent frigatebird Fregata magnificens to investigate: i) the differences in a number of physiological traits (biomarkers of blood oxidative status, corticosterone (CORT), immunity, and inflammation) between sick and healthy nestlings; and ii) whether experimentally increased intake of resveratrol (a polyphenol with antioxidant and antiviral properties) affects these physiological markers during the progress of a severe viral disease. 3. Birds with visible clinical signs showed higher oxidative damage, hemolysis and hemagglutination scores, and lower antioxidant defenses in comparison to birds without clinical signs. At the end of the experiment, supplemented birds showed: i) increased plasma haptoglobin levels and circulating antioxidant defenses; ii) reduced generation of lipid oxidative damage; and iii) negligible to no influence on immune markers, baseline CORT levels, and activity of antioxidant enzymes. 4. Our work illustrates how the availability of specific organic molecules in the diet may constrain the individuals' capacity to cope with viral infections in free-living animals.

opencc-zeroDec 2011View details →

Data from: Oxidative stress and the evolution of sex differences in lifespan and ageing in the decorated cricket, Gryllodes sigillatus

The Free Radical Theory of Ageing (FRTA) predicts that oxidative stress, induced when levels of reactive oxygen species exceed the capacity of antioxidant defences, causes ageing. Recently, it has also been argued that oxidative damage may mediate important life-history trade-offs. Here, we use inbred lines of the decorated cricket, Gryllodes sigillatus, to estimate the genetic (co)variance between age-dependent reproductive effort, lifespan, ageing, oxidative damage and total antioxidant capacity within and between the sexes. The FRTA predicts that oxidative damage should accumulate with age and negatively correlate with lifespan. We find that protein oxidation is greater in the shorter lived sex (females) and negatively genetically correlated with lifespan in both sexes. However, oxidative damage did not accumulate with age in either sex. Previously we have shown antagonistic pleiotropy between the genes for early life reproductive effort and ageing rate in both sexes, although this was stronger in females. In females, we find that elevated fecundity early in life is associated with greater protein oxidation later in life, which is in turn positively correlated with the rate of ageing. Our results provide mixed support for the FRTA but suggest that oxidative stress may mediate sex-specific life-history strategies in G. sigillatus.

Data from: Do parasites and antioxidant availability affect begging behaviour, growth rate and resistance to oxidative stress?

Early-life trade-offs faced by developing offspring can have long-term consequences for their future fitness. Young offspring use begging displays to solicit resources from their parents and have been selected to grow fast to maximize survival. However, growth and begging behaviour are generally traded-off against self-maintenance. Oxidative stress, a physiological mediator of life-history trade-offs, may play a major role in this trade-off by constraining, or being costly to, growth and begging behaviour. Yet, despite implications for the evolution of life-history strategies and parent-offspring conflicts, the interplay between growth, begging behaviour and resistance to oxidative stress remains to be investigated. We experimentally challenged wild great tit (Parus major) offspring by infesting nests with a common ectoparasite, the hen flea (Ceratophyllus gallinae), and simultaneously tested for compensating effects of increased vitamin E availability, a common dietary antioxidant. We further quantified the experimental treatment effects on offspring growth, begging intensity and oxidative stress. Flea-infested nestlings of both sexes showed reduced body mass during the first half of the nestling phase but this effect vanished short before fledging. Begging intensity and oxidative stress of both sexes were unaffected by both experimental treatments. Feeding rates were not affected by the experimental treatments but parents of flea-infested nests fed nestlings with a higher proportion of caterpillars, the main source of antioxidants. Additionally, female nestlings begged significantly less than males in control nests, while both sexes begged at similar rates in vitamin E supplemented nests. Our study shows that a parasite exposure does not necessarily affect oxidative stress levels or begging intensity, but suggests that parents can compensate for negative effects of parasitism by modifying food composition. Furthermore, our results indicate that the begging capacity of the less competitive sex is constrained by antioxidant availability.

Data from: Social rank, color morph, and social network metrics predict oxidative stress in a cichlid fish

Dominance hierarchies are a fundamental part of social systems in many species and social rank can influence access to resources and impact health and physiology. While social subordination is a profound stressor, few studies consider the social stress experienced by dominant males due to constantly needing to defend their dominance status through costly aggressive displays. Recent studies suggest that in species that use body coloration to signal status, these costs may also be color morph-specific. Our study examines the link between the social rank, intensity of territorial defense, body coloration, and oxidative stress in males of the color polymorphic cichlid fish Astatotilapia burtoni where males are either blue or yellow. We studied behavior in naturalistic communities and examined circulating reactive oxygen metabolites and antioxidant defenses. We found that dominant males experience higher concentrations of circulating reactive oxygen metabolites without notably increasing their antioxidant defenses, but this effect was not related to color morph. Aggression and social network ties predicted oxidative stress in a morph-specific manner, with yellow but not blue males showing signs of increased oxidative damage with increasing agonistic effort. In contrast to expectation, oxidative stress was not influenced by cortisol or testosterone levels. We conclude that oxidative stress is instrumental to understanding the costs and benefits of high social rank.

opencc-zeroSep 2016View details →

Data from: Marker-dependent associations among oxidative stress, growth and survival during early life in a wild mammal

Oxidative stress (OS) is hypothesized to be a key physiological mechanism mediating life-history trade-offs, but evidence from wild populations experiencing natural environmental variation is limited. We tested the hypotheses that increased early life growth rate increases OS, and that increased OS reduces first-winter survival, in wild Soay sheep (Ovis aries) lambs. We measured growth rate and first-winter survival for four consecutive cohorts, and measured two markers of oxidative damage (malondialdehyde (MDA), protein carbonyls (PC)) and two markers of antioxidant (AOX) protection (total AOX capacity (TAC), superoxide dismutase (SOD)) from blood samples. Faster lamb growth was weakly associated with increased MDA, but not associated with variation in the other three markers. Lambs with higher SOD activity were more likely to survive their first winter, as were male but not female lambs with lower PC concentrations. Survival did not vary with MDA or total TAC. Key predictions relating OS to growth and survival were therefore supported in some OS markers, but not others. This suggests that different markers capture different aspects of the complex relationships between individual oxidative state, physiology and fitness, and that overarching hypotheses relating OS to life-history variation cannot be supported or refuted by studying individual markers.

opencc-zeroDec 2018View details →

Data from: Changes in melanocyte RNA and DNA methylation favor pheomelanin synthesis and may avoid systemic oxidative stress after dietary cysteine supplementation in birds

Cysteine plays essential biological roles, but excessive amounts produce cellular oxidative stress. Cysteine metabolism is mainly mediated by the enzymes cysteine dioxygenase and γ-glutamylcysteine synthetase, respectively coded by the genes CDO1 and GCLC. Here we test a new hypothesis posing that the synthesis of the pigment pheomelanin also contributes to cysteine homeostasis in melanocytes, where cysteine can enter the pheomelanogenesis pathway. We conducted a experiment in the Eurasian nuthatch Sitta europaea, a bird producing large amounts of pheomelanin for feather pigmentation, to investigate if melanocytes show epigenetic lability under exposure to excess cysteine. We increased systemic cysteine levels in nuthatches by supplementing them with dietary cysteine during growth. This caused in feather melanocytes the downregulation of genes involved in intracellular cysteine metabolism (GCLC), cysteine transport to the cytosol from the extracellular medium (Slc7a11) and from melanosomes (CTNS), and regulation of tyrosinase activity (MC1R and ASIP). These changes were mediated by increases in DNA m5C in all genes excepting Slc7a11, which experienced RNA m6A depletion. Birds supplemented with cysteine synthesized more pheomelanin than controls, but did not suffer higher systemic oxidative stress. These results suggest that excess cysteine activates an epigenetic mechanism that favors pheomelanin synthesis and may protect from oxidative stress.

opencc-zeroDec 2015View details →

Data from: Nitric oxide signals are interlinked with calcium signals in normal pancreatic stellate cells upon oxidative stress and inflammation

The mammalian diffuse stellate cell system comprises retinoid-storing cells capable of remarkable transformations from a quiescent to an activated myofibroblast-like phenotype. Activated pancreatic stellate cells (PSCs) attract attention owing to the pivotal role they play in development of tissue fibrosis in chronic pancreatitis and pancreatic cancer. However, little is known about the actual role of PSCs in the normal pancreas. These enigmatic cells have recently been shown to respond to physiological stimuli in a manner that is markedly different from their neighbouring pancreatic acinar cells (PACs). Here, we demonstrate the capacity of PSCs to generate nitric oxide (NO), a free radical messenger mediating, for example, inflammation and vasodilatation. We show that production of cytosolic NO in PSCs is unambiguously related to cytosolic Ca2+ signals. Only stimuli that evoke Ca2+ signals in the PSCs elicit consequent NO generation. We provide fresh evidence for the striking difference between signalling pathways in PSCs and adjacent PACs, because PSCs, in contrast to PACs, generate substantial Ca2+-mediated and NOS-dependent NO signals. We also show that inhibition of NO generation protects both PSCs and PACs from necrosis. Our results highlight the interplay between Ca2+ and NO signalling pathways in cell–cell communication, and also identify a potential therapeutic target for anti-inflammatory therapies.

opencc-zeroDec 2013View details →

Data from: Oxidative stress is a potential cost of breeding in male and female northern elephant seals.

1.The trade-off between current reproductive effort and survival is a key concept of life history theory. A variety of studies support the existence of this trade-off but the underlying physiological mechanisms are not well-understood. Oxidative stress has been proposed as a potential mechanism underlying the observed inverse relationship between reproductive investment and lifespan. Prolonged fasting is associated with oxidative stress including increases in the production of reactive oxygen species, oxidative damage and inflammation. 2.Northern elephant seals (NES) undergo prolonged fasts while maintaining high metabolic rates during breeding. We investigated NES of both sexes to assess oxidative stress associated with extended breeding fasts. We measured changes in the plasma activity or concentrations of markers for oxidative stress in 30 adult male and 33 adult female northern elephant seals across their 1-3 month breeding fasts. Markers assessed included a pro-oxidant enzyme, several antioxidant enzymes, markers for oxidative damage to lipids, proteins and DNA, and markers for systemic inflammation. 3.Plasma xanthine oxidase (XO), a pro-oxidant enzyme that increases production of oxidative radicals, and several protective antioxidant enzymes increased over breeding in both sexes. Males showed increased oxidative damage to lipids and DNA and increased systemic inflammation, while oxidative damage to proteins declined across breeding. In contrast, females showed no oxidative damage to lipids or DNA or changes in inflammation, but showed increases in oxidative damage to proteins. XO activity, antioxidant enzymes, oxidative damage markers, and inflammatory markers were strongly correlated in males but these relationships were weaker or non-existent in females. 4.NES provide evidence for oxidative stress as a physiological cost of reproduction in a capital breeding mammal. Both sexes strongly up-regulated antioxidant defenses during breeding. Despite this response, and in contrast to similar duration non-breeding fasts in previous studies on conspecifics, there was evidence of oxidative damage to tissues. These data demonstrate the utility of using plasma markers to examine oxidative stress but also suggest the necessity of measuring a broad suite of plasma markers to assess systemic oxidative stress.

Data from: Effects of an early-life paraquat exposure on adult resistance to oxidative stress, plumage colour and sperm performance in a wild bird

1. Early-life stressful conditions can shape individual phenotypes and ultimately influence fitness. Oxidative stress is a pervasive threat that affects many fitness-related traits and can modulate life-history trade-offs. Yet, the extent to which exposure to oxidative stress during early life can have long-lasting effects on key fitness-related traits remains to be elucidated, particularly in natural populations of vertebrates. 2. Using a wild population of great tits Parus major, we experimentally dosed 11 day-old birds with paraquat, a pro-oxidant molecule, aiming at increasing oxidative stress. One year later, we recaptured 39 of them as adult recruiting breeders and quantified effects of the paraquat exposure on their resistance to oxidative stress, carotenoid-based plumage colouration and male sperm performance. 3. Despite the absence of a short-term effect of paraquat on oxidative stress measured two days later, the pre-fledging exposure to paraquat induced a reduction in individual oxidative damage measured at adulthood. Paraquat-dosed individuals also had brighter plumage, but no effect was observed on male sperm performance. 4. For the first time in a natural population of vertebrates, we experimentally show that an early-life acute exposure to a pro-oxidant has long-lasting effects on individual resistance to oxidative stress at adulthood. Our results are in line with the environmental matching and the hormesis hypotheses but may also reflect selective disappearance of individuals with lower resistance to oxidative stress.

opencc-by-4.0Aug 2017View details →

ROS-specific Huntingtin Interactions: Oxidative Stress Optimization 3NP

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