[Background] Theoretical models predict that a cost is necessary to guarantee honesty in begging displays given by offspring to solicit food from their parents. There is evidence for begging costs in the form of a reduced growth rate and immunocompetence. Moreover, begging implies vigorous physical activity and attentiveness, which should increase metabolism and thus the releasing of pro-oxidant substances. Consequently, we predict that soliciting offspring incur a cost in terms of oxidative stress, and growth rate and immune response (processes that generate pro-oxidants substances) are reduced in order to maintain oxidative balance. [Methodology/Principal Findings] We test whether magpie (Pica pica) nestlings incur a cost in terms of oxidative stress when experimentally forced to beg intensively, and whether oxidative balance is maintained by reducing growth rate and immune response. Our results show that begging provokes oxidative stress, and that nestlings begging for longer bouts reduce growth and immune response, thereby maintaining their oxidative status. [Conclusions/Significance] These findings help explaining the physiological link between begging and its associated growth and immunocompetence costs, which seems to be mediated by oxidative stress. Our study is a unique example of the complex relationships between the intensity of a communicative display (begging), oxidative stress, and life-history traits directly linked to viability. ; GM-R was supported by the Spanish Government (Ministerio de Ciencia y Tecnología, "Juan de la Cierva" program), and TR was supported by the Consejo Superior de Investigaciones Científicas (CSIC; Proyectos Intramurales Especiales).
Reactive oxygen species (ROS) are increasingly appreciated as down-stream effectors of cellular damage and dysfunction under natural and anthropogenic stress scenarios in aquatic systems. This comprehensive volume describes oxidative stress phenomena in different climatic zones and groups of organisms, taking into account specific habitat conditions and how they affect susceptibility to ROS damage. A comprehensive and detailed methods section is included which supplies complete protocols for analyzing ROS production, oxidative damage, and antioxidant systems. Methods are also evaluated with respect to applicability and constraints for different types of research. The authors are all internationally recognized experts in particular fields of oxidative stress research. This comprehensive reference volume is essential for students, researchers, and technicians in the field of ROS research, and also contains information useful for veterinarians, environmental health professionals, and decision makers
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Reactive oxygen species (ROS), also known as free radicals, are generated during cellular respiration. Under normal conditions, the body has the ability to neutralize the effects of free radicals by using its antioxidant defenses. In the case of an imbalance between oxidants and antioxidants, free radical production exceeds the capacity of organic combustion, resulting in oxidative stress. Of all the cellular components compromised by the harmful effects of ROS, the cell membrane is the most severely affected owing to lipid peroxidation, which invariably leads to changes in the membrane structure and permeability. With lipid peroxidation of the cell membrane, some by-products can be detected and measured in tissues, blood, and other bodily fluids. The measurement of biomarkers of oxidative stress is commonly used to quantify lipid peroxidation of the cell membrane in humans, a species in which ROS can be considered as a cause or consequence of oxidative stress-related diseases. In dogs, few studies have demonstrated this correlation. The present review aims to identify current literature knowledge relating to oxidative stress diseases and their detection in dogs.
Machine generated contents note: Preface.Acknowledgments.List of Abbreviations.Introduction to Oxidative Stress in Aquatic Ecosystems. (Doris Abele, Jose; Pablo Vázquez-Medina, Tania Zenteno-Savi;n).PART 1: Climate Regions and Special Habitats.1.1 Oxidative stress in tropical marine ecosystems (Michael P. Lesser).1.2 Oxidative challenges in polar seas (Francesco Regoli, Maura Benedetti, Andreas Krell and Doris Abele).1.3 Oxidative stress in estuarine and intertidal environments (temperate and tropical) (Carolina A. Freire, Alexis F. Welker, Janet M. Storey, Kenneth B. Storey and Marcelo Hermes-Lima).1.4 Oxidative stress tolerance strategies of intertidal macroalgae (Jose; Aguilera and Ralf Rautenberger).1.5 Oxidative stress in aquatic primary producers as a driving force for ecosystem responses to large-scale environmental changes (Pauline Snoeijs, Peter Sylvander and Norbert Ha;ubner).1.6 Migrating to the oxygen minimum layer: Euphausiids (Nelly Tremblay, Tania Zenteno-Savin, Jaime Gómez-Gutie;rrez and Alfonso N. Maeda-Marti;nez).1.7 Oxidative stress in sulphidic habitats (Joanna Joyner-Matos and David Julian).1.8 Iron in coastal marine ecosystems. Role in oxidant stress (Paula Mariela González, Dorothee Wilhelms-Dick, Doris Abele and Susana Puntarulo).1.9 Oxidative stress in coral-photobiont communities (Marco A. Liñán-Cabello,). Michael P. Lesser,).Laura A. Flores-Rami;rez, Tania Zenteno-Savi;n and Hector Reyes-Bonilla).PART 2. Aquatic Respiration and Oxygen Sensing.2.1 Principles of oxygen uptake and tissue oxygenation in water breathing animals (J.C. Massabuau and Doris Abele).2.2 Oxidative stress in sharks and rays (Roberto I. López-Cruz, Alcir Luiz Dafre and Danilo Wilhelm Filho).2.3 Oxygen Sensing: the role of ROS (Mikko Nikinmaa, Max Gassmann and Anna Bogdanova).2.4 Ischemia/reperfusion in diving birds and mammals: How they avoid oxidative damage (Tania Zenteno-Savi;n, Jose; Pablo Vázquez-Medina, Nadiezhda Cantú-Medelli;n, Paul J. Ponganis and Robert Elsner).PART 3. Marine animal models for aging, development and disease.3.1 Aging in marine animals (Eva E.R.Philipp, Julia Strahl and Alexey A. Sukhotin).3.2 Crustacean life cycles and oxidative stress (Mari;a Luisa Fanjul-Moles and Mari;a E. Gonsebatt).3.3 Transfer of free radicals between proteins and membrane lipids (Brenda Valderrama, Gustavo Rodri;guez-Alonso, and Rebecca Pogni).3.4 Immune defense of marine invertebrates -- the role of ROS and RNS (E.E.R. Philipp, S. Lipinski, J. Rast and P. Rosenstiel).3.5 Attack and defense: ROS and RNS in teleost fish immune response and the co-evolved evasion of microbes and parasites (Katja Broeg and Dieter Steinhagen).PART 4. Marine Animal Stress Response and Biomonitoring.4.1 Stress effects on metabolism and energy budgets in mollusks (Inna M. Sokolova, Alexey A. Sukhotin and Gisela Lannig).4.2 Starvation, energetics and antioxidant defenses (Amalia E. Morales, Amalia Pe;rez-Jime;nez, Miriam Furne; and Helga Guderley).4.3 Environmentally induced oxidative stress in fish (Volodymyr I. Lushchak).4.4 Chemical pollutants and the mechanisms of ROS generation in aquatic organisms (Francesco Regoli).4.5 Biomarkers of oxidative stress: benefits and drawbacks for their application in biomonitoring of aquatic environments (Jose; Monserrat, Rafaela Elias Letts, Josencler L. Ribas Ferreira, Juliane Ventura-Lima, Li;lian L. Amado, Alessandra M. Rocha, Stefania Gorbi, Raffaella Bocchetti, Maura Benedetti and Francesco Regoli).PART 5. Methods of Oxidative Stress Detection.5.1 Detection of reactive metabolites of oxygen and nitrogen (Matthew B. Grisham).5.2 Role of singlet molecular oxygen in the oxidative damage to biomolecules (Graziella Eliza Ronsein, Glaucia Regina Martinez, Eduardo Alves de Almeida, Sayuri Miyamoto, Marisa Helena Gennari de Medeiros and Paolo Di Mascio).5.3 Total oxyradical scavenging capacity, TOSC assay (Stefania Gorbi and Francesco Regoli).5.4 Spectrophotometric assays of antioxidant activities (Francesco Regoli, Raffaella Bocchetti and Danilo Wilhelm Filho).5.5 Evaluation of glutathione status in aquatic organisms (Eduardo Alves de Almeida, Danilo Grunig Humberto Silva, Afonso Celso Dias Bainy, Florêncio Porto Freitas,). Flávia Daniela Motta,). Osmar Francisco Gom).es, Marisa Helena Gennari de Medeiros and). Paolo Di Mascio).5.6 Measurement of antioxidant pigments and vitamins in phytoplankton, zooplankton and fish (Pauline Snoeijs, Norbert Ha;ubner, Peter Sylvander and Xiang-Ping Nie).5.7 Carotenoid analysis and identification in marine animals (Eduardo Alves de Almeida, Glaucia Regina Martinez, and Paolo Di Mascio).5.8 Linoleic acid oxidation products as biomarker of oxidative stress in vivo (Etsuo Niki and Yasukazu Yoshida).5.9 The classical). methods to measure oxidative damage: lipid peroxides, thiobarbituric-acid reactive substances and protein carbonyls (Volodymyr I. Lushchak, Halyna M. Semchyshyn and Oleh V. Lushchak).5.10 Protein carbonyl measurement by ELISA (Betul Catalgol, Stefanie Grimm and Tilman Grune).5.11 Chromatographic methods of malondialdehyde detection (Sayuri Miyamoto, Eduardo Alves de Almeida, Li;lian Nogueira, Marisa Helena Gennari de Medeiros and Paolo Di Mascio).5.12 The use of Electron Paramagnetic Resonance (EPR) in studies of oxidative damage to lipids in aquatic systems (Gabriela Malanga and Susana Puntarulo).5.13 The ascorbyl radical/ascorbate ratio as index of oxidative stress in aquatic organisms (Gabriela Malanga, Mari;a Bele;n Aguiar and Susana Puntarulo).5.14 Evaluation of oxidative DNA damage in aquatic animals: comet assays and 8-oxo-7,8-dihidro-2'-deoxyguanosine (8-oxodGuo) levels (Jose; Pedro Friedmann Angeli, Glaucia Regina Martinez, Flávia Daniela Motta, Eduardo Alves de Almeida, Marisa Helena Gennari de Medeiros and Paolo Di Mascio).5.15 Evaluation of DNA adducts formed by lipid peroxidation by-products (Camila Carrião Machado Garcia, Jose; Pedro Friedmann Angeli, Eduardo Alves de Almeida, Marisa Helena Gennari de Medeiros and Paolo Di Mascio).5.16 Methods to quantify lysosomal membrane stability and the accumulation of lipofuscin (Katja Broeg and Stefania Gorbi).Further reading.Index
Philasterides dicentrarchi is a free-living microaerophilic scuticociliate that can become a facultative parasite and cause a serious parasitic disease in farmed fsh. Both the free-living and parasitic forms of this scuticociliate are exposed to oxidative stress associated with environmental factors and the host immune system. The reactive oxygen species (ROS) generated by the host are neutralized by the ciliate by means of antioxidant defences. In this study we aimed to identify metalloenzymes with superoxide dismutase (SOD) activity apable of inactivating the superoxide anion (•O2−) generated during induction of oxidative stress. P. dicentrarchi possesses the three characteristic types of SOD isoenzymes in eukaryotes: copper/zinc-SOD, manganese-SOD and iron-SOD. The Cu/Zn-SOD isoenzymes comprise three types of homodimeric proteins (CSD1-3) of molecular weight (MW) 34–44kDa and with very diferent AA sequences. All Cu/Zn-SODs are sensitive to NaCN, located in the cytosol and in the alveolar sacs, and one of them (CSD2) is extracellular. Mn- and Fe-SOD transcripts encode homodimeric proteins (MSD and FSD, respectively) in their native state: a) MSD (MW 50kDa) is insensitive to H2O2 and NaN3 and is located in the mitochondria; and b) FSD (MW 60kDa) is sensitive to H2O2, NaN3 and the polyphenol trans-resveratrol and is located extracellularly. Expression of SOD isoenzymes increases when •O2 − is induced by ultraviolet (UV) irradiation, and the increase is proportional to the dose of energy applied, indicating that these enzymes are actively involved in cellular protection against oxidative stress ; This study was financially supported by grant AGL2017-83577-R awarded by the Ministerio de Economía y Competitividad (Spain) and Fondo Europeo de Desarrollo Regional -FEDER- (European Union), by grant ED431C2017/31 from the Xunta de Galicia (Spain), and by PARAFISHCONTROL project, which received funding from the European Union's Horizon 2020 research and innovation programme under grant agreement No. 634429 ; SI
Obesity is a multifactorial disease characterized by the excessive accumulation of fat in adipose tissue and peripheral organs. Its derived metabolic complications are mediated by the associated oxidative stress, inflammation and hypoxia. Oxidative stress is due to the excessive production of reactive oxygen species or diminished antioxidant defenses. Genetic variants, such as single nucleotide polymorphisms in antioxidant defense system genes, could alter the efficacy of these enzymes and, ultimately, the risk of obesity; thus, studies investigating the role of genetic variations in genes related to oxidative stress could be useful for better understanding the etiology of obesity and its metabolic complications. The lack of existing literature reviews in this field encouraged us to gather the findings from studies focusing on the impact of single nucleotide polymorphisms in antioxidant enzymes, oxidative stress-producing systems and transcription factor genes concerning their association with obesity risk and its phenotypes. In the future, the characterization of these single nucleotide polymorphisms (SNPs) in obese patients could contribute to the development of controlled antioxidant therapies potentially beneficial for the treatment of obesity-derived metabolic complications. ; The present study was funded by the Instituto de Salud Carlos III-Fondo de Investigación Sanitaria (FIS) (project number: PI11/02042 and PI05/1968); Redes temáticas de investigación cooperativa (RETIC), Research Network on Maternal and Child Health and Development (SAMID) RD08/0072/0028 and SAMID RD12/0026/0015; Junta de Andalucía, Consejería de Innovación y Ciencia (project number: P06-CTS 2203 and PI-0296/2007). Rupérez A.I was funded by a Formación de Profesorado Universitario (FPU) stipend from the Ministry of Education and Science of the Spanish Government (AP2009-0547).
In: Ecotoxicology and environmental safety: EES ; official journal of the International Society of Ecotoxicology and Environmental safety, Band 94, S. 153-163
In: Ecotoxicology and environmental safety: EES ; official journal of the International Society of Ecotoxicology and Environmental safety, Band 188, S. 109878
The present study analyzed experimentally the association between the experience of psychological stress and the physiological stress response of prospective teachers. The experienced stress was assessed by self-reported data. Cortisol concentrations via saliva samples reflected the physiological response. The results show no difference between the stress and the control group in the experience of psychological stress. However, the stress group had significantly increased cortisol concentrations compared to the control group. The study could not show any correlation between the two stress parameters. The results suggest that a stress response should be validated based not only on the experience of psychological stress but also on the physiological stress response. This is particularly crucial in light of the fact that the majority of studies concerning stress in teachers are limited to experiences of psychological stress so far. Due to this, the results may provide a first important contribution to a more comprehensive stress assessment for teachers.
Heatstroke (HS) is an acute, progressive life-threatening emergency. Animals, including military working dogs (IDFMWD), rapidly activate cytoprotective processes, e.g., heat shock proteins (HSPs) and antioxidative molecules, in response to heat stress. We hypothesized that serum HSPs (eHSP72) and oxidative stress markers would differ in IDFMWD with a history of HS compared with controls and thus could be used to detect susceptibility to recurrent HS. eHSPs concentration, oxidative stress markers, and systemic physiological parameters were studied in dogs with and without histories of HS, undergoing indoor or outdoor training. Treadmill physical performance tests (PPTs) were conducted indoors at 22 °C (groups C-I and HS-I) or outdoors under heat stress conditions of 36 °C; 60% humidity (groups C-O and HS-O). Pre-, immediately post-, and 45 min post-PPT heart rate (HR), respiratory rate, and rectal temperature (T(re)) were recorded in all dogs. Likewise, blood samples were collected and eHSP72, venous blood gas analysis, and lactate and creatine kinase activity (CK) were assayed. Serum uric acid (sUA) and total serum redox potential (TRP) were measured only in the indoor group. Immediately post-PPT under both environmental conditions, T(re), HR, eHSP, sUA, and TRP (only measured in indoor PPT) significantly (P < 0.05) increased, whereas venous blood pH and bicarbonate decreased significantly (P < 0.05). Between groups comparisons demonstrated significant differences in basal HR and post-PPT T(re) immediately after outdoor PPT. eHSP72 induction, CK, sUA, and serum TRP remained significantly higher in the HS group during post-PPT recovery. Taken together, animals with a history of HS have different results, and this signature of previous HS may predict altered heat sensitivity.
Im Rahmen der Studie BundeswehrEinsatz und STress (BEST) wurde die Entstehung von Desoxyribonukleinsäure (DNA)-Strangbrüchen durch mentalen Stress in Vollblutproben von Soldaten (Stichprobengröße n = 72) mithilfe des Comet Assay untersucht. Mentalen Stress erfuhren die Probanden im Trierer Social Stress Test for Groups (TSST-G), bei dem die Vollblutproben vor, direkt nach Stressexposition und nach anschließender Ruhephase entnommen wurden und währendessen wurden von den Probanden der Multidimensionale Befindlichkeitsfragebogen (MDBF), der Fragebogen für Zustandsangst des State-Trait-Angstinventars (STAI-S) und der Fragebogen für Primary Appraisal Secondary Apprasial (PASA) zur Erhebung des subjektiven Stress ausgefüllt. Das kardiovaskuläre Risiko der Probanden wurde durch den Risikoscore der Prospective Cardiovascular Munster (PROCAM) Studie berechnet. Es konnte ein Anstieg der DNA-Strangbrüche unter mentalem Stress sowie ein Abfall der Schäden während der Ruhephase festgestellt werden. Geschlechterspezifische Unterschiede fanden sich nicht. Die Probandengruppe mit kardiovaskulärem Risiko zeigte eine signifikant höhere Menge an DNA-Strangbrüchen unter mentalem Stress gegenüber den Probanden ohne positivem Risikoscore. Dabei zeigten die Parameter positive Familienanamnese sowie die Blutfettwerte (High density Lipoprotein (HDL)-Cholesterin, Low density Lipoprotein (LDL)-Cholesterin und Triglyceride) den größten Zusammenhang zu der Anzahl an DNA-Strangbrüchen. Die Fragebögen zum subjektiven Stress korrelierten nicht mit der Menge an DNA-Strangbrüchen.