Oxidative costs of cooperation in cooperatively breeding Damaraland mole-rats

Within cooperatively breeding societies, individuals adjust cooperative contributions to maximize indirect fitness and minimize direct fitness costs. Yet, little is known about the physiological costs of cooperation, which may be detrimental to direct fitness. Oxidative stress, the imbalance between reactive oxygen species (by-products of energy production) and antioxidant protection, may represent such a cost when cooperative behaviours are energetically demanding. Oxidative stress can lead to the accumulation of cellular damage, compromising survival and reproduction, thus mediating the trade-off between these competing life-history traits. Here, we experimentally increased energetically demanding cooperative contributions in captive Damaraland mole-rats ( Fukomys damarensis ). We quantified oxidative stress-related effects of increased cooperation on somatic and germline tissues, and the trade-off between them. Increased cooperative contributions induced oxidative stress in females and males, without increasing somatic damage. Males accumulated oxidative damage in their germline despite an increase in antioxidant defences. Finally, oxidative damage accumulation became biased towards the germline, while antioxidant protection remained biased towards the soma, suggesting that males favour the maintenance of somatic tissues (i.e. survival over reproduction). Our results show that heightened cooperative contributions can ultimately affect direct fitness through oxidative stress costs, which may represent a key selective pressure for the evolution of cooperation.

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Effects of Caloric Restriction on Cardiac Oxidative Stress and Mitochondrial Bioenergetics: Potential Role of Cardiac Sirtuins

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/528935 ◽

2013 ◽

Vol 2013 ◽

pp. 1-11 ◽

Cited By ~ 29

Author(s):

Ken Shinmura

Keyword(s):

Oxidative Stress ◽

Free Radical ◽

Oxidative Damage ◽

Caloric Restriction ◽

Functional Decline ◽

Cellular Damage ◽

Free Radical Theory ◽

Radical Theory ◽

Stress Theory

The biology of aging has not been fully clarified, but the free radical theory of aging is one of the strongest aging theories proposed to date. The free radical theory has been expanded to the oxidative stress theory, in which mitochondria play a central role in the development of the aging process because of their critical roles in bioenergetics, oxidant production, and regulation of cell death. A decline in cardiac mitochondrial function associated with the accumulation of oxidative damage might be responsible, at least in part, for the decline in cardiac performance with age. In contrast, lifelong caloric restriction can attenuate functional decline with age, delay the onset of morbidity, and extend lifespan in various species. The effect of caloric restriction appears to be related to a reduction in cellular damage induced by reactive oxygen species. There is increasing evidence that sirtuins play an essential role in the reduction of mitochondrial oxidative stress during caloric restriction. We speculate that cardiac sirtuins attenuate the accumulation of oxidative damage associated with age by modifying specific mitochondrial proteins posttranscriptionally. Therefore, the distinct role of each sirtuin in the heart subjected to caloric restriction should be clarified to translate sirtuin biology into clinical practice.

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The Redox System inC. elegans, a Phylogenetic Approach

Journal of Toxicology ◽

10.1155/2012/546915 ◽

2012 ◽

Vol 2012 ◽

pp. 1-20 ◽

Cited By ~ 12

Author(s):

Andrew D. Johnston ◽

Paul R. Ebert

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Cellular Damage ◽

Future Research ◽

Homologous Proteins ◽

Redox Biology ◽

Redox Signalling ◽

C Elegans ◽

Age Related

Oxidative stress is a toxic state caused by an imbalance between the production and elimination of reactive oxygen species (ROS). ROS cause oxidative damage to cellular components such as proteins, lipids, and nucleic acids. While the role of ROS in cellular damage is frequently all that is noted, ROS are also important in redox signalling. The “Redox Hypothesis" has been proposed to emphasize a dual role of ROS. This hypothesis suggests that the primary effect of changes to the redox state is modified cellular signalling rather than simply oxidative damage. In extreme cases, alteration of redox signalling can contribute to the toxicity of ROS, as well as to ageing and age-related diseases. The nematode speciesCaenorhabditis elegansprovides an excellent model for the study of oxidative stress and redox signalling in animals. We use protein sequences from central redox systems inHomo sapiens,Drosophila melanogaster, andSaccharomyces cerevisiaeto query Genbank for homologous proteins inC. elegans. We then use maximum likelihood phylogenetic analysis to compare protein families betweenC. elegansand the other organisms to facilitate future research into the genetics of redox biology.

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Effect of Oxidative Stress on Lymphocytes from Elderly Subjects

Clinical Science ◽

10.1042/cs0940447 ◽

1998 ◽

Vol 94 (4) ◽

pp. 447-452 ◽

Cited By ~ 11

Author(s):

E. García-Arumí ◽

A. L. Andreu ◽

J. López-Hellín ◽

S. Schwartz

Keyword(s):

Oxidative Stress ◽

Enzyme Activity ◽

Oxidative Damage ◽

Antioxidant Enzyme ◽

Antioxidant Enzyme Activity ◽

Elderly Subjects ◽

Antioxidant Enzyme Activities ◽

Antioxidant Defences ◽

Protein Carbonyl Content ◽

Healthy Elderly

1. Oxidative damage has been associated with ageing, but there is no agreement as to whether or not it is produced by a decrease in antioxidant defences with the ageing process. In purified lymphocytes from 47 healthy elderly (75.27 ± 0.91 years) and 47 healthy young (29.87 ± 0.53 years) volunteers, we studied the levels of antioxidant enzyme activity (superoxide dismutase, catalase and glutathione peroxidase), protein oxidative damage (as protein carbonyl content) and lysosomal proteolytic activity (cathepsins B, H and L), with and without exposure to oxidative stress produced by 25 μmol/l H2O2. 2. There were no differences in antioxidant enzyme activities in the stressed and non-stressed samples between the young and elderly subjects, indicating that there was no relationship between age and antioxidant enzyme activity even in oxidative stress. However, a dissimilar response to oxidative stress was observed in protein oxidative damage and cathepsin B and L activities, depending on the age of the donor. 3. With these results we conclude that oxidative stress produces greater protein oxidative damage and increased protein degradation in elderly subjects than in young ones; this effect cannot be attributed to dissimilar antioxidant enzyme responses to oxidative stress, since these did not differ between the two age groups.

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Nrf2 mediated ER-phagy protects against oxidative damage in intervertebral disc degeneration

10.1101/2021.11.21.469451 ◽

2021 ◽

Author(s):

zhen lin ◽

libin ni ◽

cheng teng ◽

zhao zhang ◽

xinlei lu ◽

...

Keyword(s):

Oxidative Stress ◽

Intervertebral Disc ◽

Oxidative Damage ◽

Er Stress ◽

Disc Degeneration ◽

Intervertebral Disc Degeneration ◽

Cellular Damage ◽

Nucleus Pulposus Cells

Intervertebral disc degeneration (IDD) increases the risk of low back pain (LBP). Oxidative stress may induce cellular damage and contribute to various diseases including IDD. Endoplasmic reticulum autophagy (ER-phagy) is a specific type of autophagy, its role in oxidative stress induced damage as well as in IDD is unknown. This study explores the role of ER-phagy in oxidative damage in intervertebral disc nucleus pulposus cells (NPCs), as well as the Nrf2/FAM134B axis in ER-phagy regulation and IDD therapy. We found ER-phagy was decreased in NPCs during oxidative stress; while FAM134B may promote ER-phagy and alleviate oxidative stress induced ER-stress and apoptosis. In addition, the nuclear transcription factor Nrf2 may promote the expression of FAM134B as well as ER-phagy, and suppress ER-stress and apoptosis in NPCs. Furthermore, overexpression of FAM134B and Nrf2 could effectively attenuate the progression of IDD in rats in vivo. These results suggest Nrf2/FAM134B mediated ER-phagy may combat oxidative damage in cells; meanwhile, ER-phagy as well as Nrf2 could be potential therapeutic targets for IDD.

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Metals as a cause of oxidative stress in fish: a review

Veterinární Medicína ◽

10.17221/4272-vetmed ◽

2011 ◽

Vol 56 (No. 11) ◽

pp. 537-546 ◽

Cited By ~ 139

Author(s):

M. Sevcikova ◽

H. Modra ◽

A. Slaninova ◽

Z. Svobodova

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Oxidative Damage ◽

Metal Binding ◽

Special Functions ◽

Current Knowledge ◽

Reactive Oxygen ◽

Enzyme Inactivation ◽

Oxygen Species ◽

Antioxidant Defences

This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment.  

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Yolk testosterone reduces oxidative damages during postnatal development

Biology Letters ◽

10.1098/rsbl.2010.0421 ◽

2010 ◽

Vol 7 (1) ◽

pp. 93-95 ◽

Cited By ~ 25

Author(s):

José Carlos Noguera ◽

Carlos Alonso-Alvarez ◽

Sin-Yeon Kim ◽

Judith Morales ◽

Alberto Velando

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Postnatal Development ◽

Early Development ◽

Early Life ◽

Antioxidant Defences ◽

Oxidative Damages ◽

Plasma Antioxidant ◽

Yolk Testosterone

Conditions experienced during early life can influence the development of an organism and several physiological traits, even in adulthood. An important factor is the level of oxidative stress experienced during early life. In birds, extra-genomic egg substances, such as the testosterone hormone, may exert a widespread influence over the offspring phenotype. Interestingly, testosterone can also upregulate the bioavailability of certain antioxidants but simultaneously increases the susceptibility to oxidative stress in adulthood. However, little is known about the effects of maternally derived yolk testosterone on oxidative stress in developing birds. Here, we investigated the role of yolk testosterone on oxidative stress of yellow-legged gull chicks during their early development by experimentally increasing yolk testosterone levels. Levels of antioxidants, reactive oxygen species and lipid oxidative damage were determined in plasma during nestlings' growth. Our results revealed that, contrary to control chicks, birds hatched from testosterone-treated eggs did not show an increase in the levels of oxidative damage during postnatal development. Moreover, the same birds showed a transient increase in plasma antioxidant levels. Our results suggest that yolk testosterone may shape the oxidative stress-resistance phenotype of the chicks during early development owing to an increase in antioxidant defences and repair processes.

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Heat treatment reduces oxidative stress and protects muscle mass during immobilization

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00497.2004 ◽

2005 ◽

Vol 289 (1) ◽

pp. R134-R139 ◽

Cited By ~ 91

Author(s):

Joshua T. Selsby ◽

Stephen L. Dodd

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Muscle Mass ◽

Control Group ◽

Antioxidant Enzyme Activities ◽

Antioxidant Protection ◽

Disuse Atrophy ◽

The Core ◽

Group A

This study examined the role of heating on oxidative stress and muscle mass in immobilized limbs. Rats were divided into three groups ( n = 9/group): a control group (Con), an immobilized group (Im), and an immobilized and heated group (ImH). Rats were immobilized in the plantarflexed position for 8 days. The core temperature of the ImH group was elevated to 41–41.5°C on alternating days and maintained for 30 min before cooling. On day 8, both heat shock protein 25 (HSP25) and HSP72 were markedly elevated in the ImH compared with the Im group, whereas results in the Im group were not different from Con. Most notably, the ImH group had significantly larger solei compared with the Im group, which were less than those shown in the Con group. Furthermore, immobilization alone caused a significant increase in oxidative damage, and the addition of heating to immobilization significantly reduced oxidative damage. In an effort to further identify the cause of this protective effect, antioxidant enzyme activities were assessed. CuZnSOD was sharply elevated in Im compared ( P < 0.025) with that in the Con and reduced in the ImH group compared with that in the Im group ( P < 0.025). Catalase was elevated 8% ( P < 0.025) in the Im group compared with the Con group and was similar to the ImH group. Glutathione peroxidase, glutathione reductase, and MnSOD did not differ between groups. These data indicate that heating provides protection against oxidative stress and preserves muscle mass during disuse atrophy. These data also suggest that antioxidant protection is not conferred via antioxidant enzymes, and HSPs may play an important role.

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DHA Protects Hepatocytes from Oxidative Injury through GPR120/ERK-Mediated Mitophagy

International Journal of Molecular Sciences ◽

10.3390/ijms22115675 ◽

2021 ◽

Vol 22 (11) ◽

pp. 5675

Author(s):

Jinglong Chen ◽

Danping Wang ◽

Yibo Zong ◽

Xiaojing Yang

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Mitochondrial Dysfunction ◽

Liver Diseases ◽

Antioxidant Effect ◽

Cellular Damage ◽

Autophagic Flux

Oxidative stress occurs in a variety of clinical liver diseases and causes cellular damage and mitochondrial dysfunction. The clearance of damaged mitochondria by mitophagy may facilitate mitochondrial biogenesis and enhance cell survival. Although the supplementation of docosahexaenoic acid (DHA) has been recognized to relieve the symptoms of various liver diseases, the antioxidant effect of DHA in liver disease is still unclear. The purpose of our research was to investigate the antioxidant effect of DHA in the liver and the possible role of mitophagy in this. In vitro, H2O2-induced injury was caused in AML12 cells. The results showed that DHA repressed the level of reactive oxygen species (ROS) induced by H2O2 and stimulated the cellular antioxidation response. Most notably, DHA restored oxidative stress-impaired autophagic flux and promoted protective autophagy. In addition, PINK/Parkin-mediated mitophagy was activated by DHA in AML12 cells and alleviated mitochondrial dysfunction. The ERK1/2 signaling pathway was inhibited during oxidative stress but reactivated by DHA treatment. It was proven that the expression of ERK1/2 was involved in the regulation of mitophagy by the ERK1/2 inhibitor. We further proved these results in vivo. DHA effectively alleviated the liver oxidative damage caused by CCl4 and enhanced antioxidation capacity; intriguingly, autophagy was also activated. In summary, our data demonstrated that DHA protected hepatocytes from oxidative damage through GPR120/ERK-mediated mitophagy.

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ZnO Nanoparticles Alter Redox Metabolism of Limnoperna Fortunei

10.21203/rs.3.rs-210424/v1 ◽

2021 ◽

Author(s):

Francine Girardello ◽

Camila Custódio Leite ◽

Luciana Bavaresco Touguinha ◽

Mariana Roesch-Ely ◽

Andreia Neves Fernandes ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Oxidative Damage ◽

Wide Distribution ◽

Ecological Impacts ◽

Antioxidant Defences ◽

Redox Metabolism ◽

Enzymatic Antioxidant ◽

South Of Brazil ◽

Golden Mussel

Abstract Nanoparticles incorporated in consumer and industrial products cause concerns about their potential ecological impacts. Zinc oxide nanoparticles (ZnO-NP) have several applications, which increases their potential for release to the environment, causing ecotoxicological problems. Bivalve mollusks are susceptible targets for nanoparticles toxicity, since nanomaterials can enter the cells by endocytosis mechanisms. Limnoperma fortunei (golden mussel) are validated for biomonitoring purposes and have a wide distribution in the South of Brazil, where it can be collected throughout the year. The aim of this study was to evaluate the influence of ZnO-NP on the redox metabolism by enzymatic and non-enzymatic antioxidant defense assessment in addition to DNA damage by DNA fragmentation assay in L. fortunei after exposure to ZnO-NP. Adult bivalves were placed in contact with 1, 10, and 50 µg mL-1 ZnO-NP during three incubation times: 2, 4 and 24 h. Ionic Zn release, enzymatic and non-enzymatic antioxidant activity, oxidative damage to lipids and proteins and DNA damage were evaluated. Oxidative damage to proteins and lipids were observed after 4 h exposure and returned to baseline levels after 24 h. Superoxide dismutase levels decreased after 4 h exposure and increased after 24 h. No significant alteration was observed in catalase activity or even DNA double strand cleavage. The dissociation of ZnO may occur after 24 h, releasing ionic zinc (Zn2+) by hydrolysis, which was confirmed as the ionic Zn concentration increased following 24 h exposure. In conclusion, ZnO-NP were able to induce oxidative stress in exposed golden mussels. The golden mussel is capable to modulate its own antioxidant defences in response to oxidative stress and seems to be able to hydrolyse the nanoparticle and consequently release Zn2+ into the cellular compartment.

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The evolution of life history strategies in plants and its relationship to the evolution of protective cellular mechanisms against reactive oxygen species

10.21203/rs.3.rs-632316/v1 ◽

2021 ◽

Author(s):

Abraam Zakhary ◽

Aashika Nagarajan ◽

Charlotte Ngo ◽

Marwa Saidajan ◽

Supreet Babbar ◽

...

Keyword(s):

Oxidative Stress ◽

Life History ◽

Oxidative Damage ◽

Chlorophyll A ◽

Cellular Damage ◽

Life History Strategies ◽

Ancestral State ◽

Chlorophyll B ◽

Cellular Mechanisms ◽

Perennial Plants

Abstract Purpose. The Oxidative Stress Theory of Aging (OSTA) states that accumulation of oxidative damage is a major contributor to aging; however, until now, no studies have examined whether perennial plants exhibit cellular mechanisms to better protect themselves against oxidative damage than annual plants, nor how these mechanisms may have evolved. Methods. We undertook three approaches to evaluate the capacity for annual and perennial plants to resist oxidative damage. The first approach involved using an electrolyte leakage assay to assess the rate of cellular damage in leaves exposed to exogenous H 2 O 2 . The second approach involved determining the concentration of exogenous H 2 O 2 required to maximize germination rates, which provides insight about the antioxidant levels in seeds. The third approach involved assessing the susceptibility of chlorophyll a and chlorophyll b to exogenous H 2 O 2 and determining chlorophyll a/b ratios. We also conducted an ancestral state reconstruction of life history strategies in order to interpret our results in an evolutionary context. Results. Leaves from deciduous and evergreen perennials showed a lower rate of cellular damage than leaves from annuals when exposed to exogenous H 2 O 2 . Seeds from deciduous perennials—but not biennials or evergreen perennials—required a higher H 2 O 2 concentration to maximize germination rate compared to seeds from annuals, suggesting that seeds from deciduous perennials have higher antioxidant levels. Although chlorophyll b was found to be more susceptible to damage from exogenous H 2 O 2 , chlorophyll a/b ratios did not differ among life history strategies. Ancestral state reconstruction revealed that the ancestral plant was most likely an evergreen perennial. Conclusion. Our results showcase that resistance to oxidative stress is necessary for perennial plants to survive over multiple years. The mechanisms responsible for the increased tolerance of perennial species to oxidative stress has not been fully elucidated by this study, but it does not involve changes to chlorophyll a/b ratios, as such changes could disrupt photosynthesis. The developmental onset of these protective mechanisms was delayed in evergreen perennials compared to deciduous perennials, perhaps because the ancestral evergreens were primarily focused on rapid colonization of the terrestrial environment, which requires faster germination rates induced by higher H 2 O 2 levels.

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