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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.

14. AGING IN MARINE ANIMALS15. OXIDATIVE STRESS AND ANTIOXIDANT SYSTEMS IN CRUSTACEAN LIFE CYCLES; 16. TRANSFER OF FREE RADICALS BETWEEN PROTEINS AND MEMBRANE LIPIDS: IMPLICATIONS FOR AQUATIC BIOLOGY; 17. IMMUNE DEFENSE OF MARINE INVERTEBRATES: THE ROLE OF REACTIVE OXYGEN AND NITROGEN SPECIES; 18. ATTACK AND DEFENSE: REACTIVE OXYGEN AND NITROGEN SPECIES IN TELEOST FISH IMMUNE RESPONSE AND THE COEVOLVED EVASION OF MICROBES AND PARASITES; PART IV. MARINE ANIMAL STRESS RESPONSE AND BIOMONITORING; 19. STRESS EFFECTS ON METABOLISM AND ENERGY BUDGETS IN MOLLUSKS

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).

Intro -- Oxidative Stress and the Critically Ill Patient -- Oxidative Stress and the Critically Ill Patient -- Library of Congress Cataloging-in-Publication Data -- Contents -- Introduction -- Chapter I: Free Radicals: An Overview -- Abstract -- Abbreviations -- 2. Introduction -- 3. Types of Free Radicals -- 3.1. Reactive Oxygen Species -- a) Superoxide (O2−) -- b) Hydrogen peroxide (H2O2) -- c) Hydroxyl Radical (OH) -- 3.2. Reactive Nitrogen Species -- 4. Sources of Free Radicals -- a) "Accidental" Generation -- b) Deliberate Synthesis -- 4.1. Mitochondria -- 4.2. NADPH -- 4.3. Xanthine Oxidase -- 4.4. Metal-Mediated Generation of ROS -- 4.5. Nitric Oxide Synthase -- 4.6. Mieloperoxidase -- 4.7. Cytochrome P450 -- 5. In Vivo Effects of Free Radicals -- 5.1. Physiological Functions -- 5.2. Pathophysiological Effects -- Oxidative Damage -- 6. Antioxidant Defense Systems -- and Oxidative Stress -- 7. Biomarkers of Oxidative Stress -- 8. Oxidative Stress and Diseases -- 8.1. Cardiovascular Diseases -- 8.2. Hypertension -- 8.3. Atherosclerosis -- 8.4. Metabolic Syndrome and Diabetes -- 8.5. Neurodegenerative Diseases -- 8.6. Cancer -- 8.7. Rheumatoid Arthritis -- 8.8. Aging -- Conclusion -- References -- Chapter II: Pathophysiology of Sepsis and Septic Shock -- Abstract -- Abbreviations -- 2. Introduction -- 3. Pathophysiology of Sepsis -- 3.1. Basic Molecular Mechanisms of Inflammation in Sepsis -- 3.1.1. Pathogen-Host Interaction -- 3.1.2. Neutrophils -- 3.1.3. Cytokines -- 3.1.4. Coagulation Disorders in Sepsis -- 3.1.5. Endothelial Cells -- 3.1.6. Complement Activation -- 3.2. Immunoparalysis -- 4. Pathophysiology of Septic Shock -- Conclusions and Future Goals -- References -- Chapter III: Inflammation -- Abstract -- Abbreviations -- 2. Introduction -- 3. Current Concepts of the Inflammatory Response -- 3.1. Cellular Mediators.

Yeasts, such as Saccharomyces cerevisiae, have long served as useful models for the study of oxidative stress, an event associated with cell death and severe human pathologies.This reviewwill discuss oxidative stress in yeast, in terms of sources of reactive oxygen species (ROS), their molecular targets, and the metabolic responses elicited by cellular ROS accumulation. Responses of yeast to accumulated ROS include upregulation of antioxidants mediated by complex transcriptional changes, activation of pro-survival pathways such as mitophagy, and programmed cell death (PCD) which, apart from apoptosis, includes pathways such as autophagy and necrosis, a form of cell death long considered accidental and uncoordinated. The role of ROS in yeast aging will also be discussed. ; Work in the authors' laboratory is partly funded by the Malta Government Scholarship Scheme (MGSS) award, fund number ME 367/07/8, to Gianluca Farrugia and partly by Research Fund grants to Rena Balzan from the University of Malta. ; peer-reviewed

Toxic substances generated during the metabolism of alcohol in the liver may contribute to the development of alcoholic liver disease. These substances include highly reactive molecules that can destroy vital cell components through a process called oxidation. Cells are protected against oxidation by the action of certain enzymes, vitamins, and other substances, known collectively as antioxidants. An imbalance between oxidants and antioxidants can lead to oxidative stress, characterized by escalating cell damage. Evidence suggests that the major energy-generating structures within cells (i.e., mitochondria) may be especially sensitive to oxidative stress, resulting in diminished energy production. Medications that reduce oxidative stress in mitochondria may ameliorate liver disease. ; The work presented in this review was supported by National Institute of Alcohol Abuse and Alcoholism grant AA09526, Direccion General Politica Cientifica y Tecnica grant PM 95–0185, Fondo Investigaciones Sanitarias grant FISS 94–0046/01, Plan Nacional de I+D grant SAF 97–0087–C01, and Europharm ; Peer Reviewed

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.

Contribution of oxidative stress to neurodegenerative disease
Paul A. Hyslop, from Arkley BioTek Indianapolis, details an ongoing specific research approach to identify, characterize, and validate physiologically relevant neuronal targets of H2O2 in designing therapeutics for neurodegenerative disease progression. The societal impact of dementia resulting from the major neurodegenerative diseases such as Alzheimer's presents a growing and significant unmet medical need. (1) Various cellular metabolic and structural deficits, neuroinflammation, and oxidative stress are known to result in the progressive loss of vulnerable non-regenerative neurons. (2)

Abstract
Background One of the antioxidant mechanisms is the dynamic balance between thiol and disulfide, which, in subarachnoid hemorrhage and other chronic diseases, is disrupted in favor of the latter. The two most commonly used oxidative stress (OS) biochemical markers are the oxidative stress index (OSI) value, which indicates the total oxidant status (TOS) and total antioxidant status (TAS) balance, and the thiol–disulfide (TDS) value, which indicates the total thiol (TT) and native thiol (NT) balance. High OS levels require further investigations. We aimed to investigate the OS level in aneurysmal SAH (aSAH) patients.
methods In this clinical prospective study, blood samples were collected from 50 consecutively treated patients with aSAH and 50 volunteers. Serum TOS, TAS, TT, and NT levels were measured using Erel's method via a spectrophotometer. The Glasgow Coma Scale (GCS) scores, Fisher grades, length of hospital stay (LOS), and the Glasgow Outcome Scale (GOS) scores were recorded. Consequently, the OSI and TDS values were calculated in all participants.
Results A statistically significant difference was observed in the TAS, TOS, OSI, and TDS values between the aSAH patients and the controls. The TT and NT values were significantly lower in aSAH patients than in the controls. A correlation was identified between the OSI values and the GCS scores. Although a correlation was observed between the TDS values and the LOS, no correlation was found between the OSI and the TDS values.
Conclusion The OSI and TDS, which are OS indicators, might serve as the additional objective nominal data to evaluate the treatment efficacy and follow-up for SAH patients. Moreover, decreasing the OSI values and increasing the TT values can be used as improvement indicators in the treated aSAH patients. If we can reduce the OS at the early stage of SAH, it could improve the prognosis by reducing both the morbidity and mortality rates. Further randomized investigations are required to prove the findings in this prospective study.