Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q8IXL6 (RNS)
 1,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of antioxidative enzymes are regulated by gene expressions as well as by post-translational modifications. Although their functions are to scavenge reactive oxygen (ROS) and nitrogen species (RNS), they may also be targets of various oxidants. When ROS and RNS modify the functions of antioxidative enzymes, especially glutathione peroxidase, they may induce apoptotic cell death in susceptible cells. It is conceivable, therefore, that at least a part of the apoptotic pathways mediated by ROS and RNS may be associated with modification of the redox regulation of cellular functions due to elevations of such substances. In this article we review recent findings about the effects of various oxidative conditions associated with alteration of these antioxidative enzymes and the concomitant cellular damage induced.
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PMID:Down regulation of superoxide dismutases and glutathione peroxidase by reactive oxygen and nitrogen species. 1051 34

Reactive oxygen (ROS) and nitrogen species (RNS) are continuously generated in the biological system and play an important role in a variety of physiological and pathological processes. There is evidence that physical exercise augments the generation of ROS/RNS. The present review discusses and compares insights into the generation and function of ROS/RNS such as superoxide, hydrogen peroxide, hypochloric acid, and nitric oxide released by leukocytes in response to exercise. Emphasis is placed on: (a) mechanisms and regulation of ROS/RNS generation in immunocompetent cells with respect to acute exercise and regular training; (b) damaging effects of ROS/RNS in terms of oxidative stress which may be causally involved in features such as exercise-induced damage to muscle tissue and leukocyte DNA; (c) (immuno-) modulating effects of ROS/RNS which include activation of transcription factors; (d) responses of antioxidant stress proteins to acute exercise and regular training; and (e) effects of antioxidants on exercise-induced changes in immune function. Available data suggests that ROS/RNS are involved in the inflammatory response to heavy exercise and therefore exert damaging effects. Several immune functions are influenced by actions of ROS/RNS, and it is hypothesized that adaption to regular training is also modulated in part by free radicals. Furthermore, regular training seems to reduce the capacity of leukocytes for oxidant release and leads to an adaptation of antioxidative mechanisms, which may contribute to a limitation of exercise-induced oxidative stress.
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PMID:Free radicals and oxidative stress in exercise--immunological aspects. 1051 61

It is clear that smoking causes an increase in free radicals, reactive nitrogen and oxygen species (RNS and ROS, respectively), and that cigarette smoking is associated with increases in the incidence and severity of several diseases including atherosclerosis, cancer, and chronic obstructive lung disease. Although there is still no unequivocal evidence that oxidative stress is a contributor to these diseases or that an increased intake of antioxidant nutrients is beneficial, the observation that smokers have lower circulating levels of some of these nutrients, raises concern. This article discusses the possible links between the observed oxidant-induced damage related to tobacco smoking, effects on cellular mechanisms, and their potential involvement in the causation and enhancement of disease processes.
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PMID:Tobacco-related diseases. Is there a role for antioxidant micronutrient supplementation? 1076 98

In this present paper the age-induced effect on reactive oxidizing species generated by oxygen (ROS) and nitrogen (RNS) was studied using human phagocyting granulocytes. The ROS and RNS were quantified, respectively, in a chemiluminescence assay and by the measurement of nitrite production. The age-induced reactive oxidizing species generation was studied in healthy subjects ranging from 20 to 80 years old, divided into six age groups: group I, 20-29 years old; group II, 30-39 years old; group III, 40-49 years old; group IV, 50-59 years old; group V, 60-69 years old; and group VI, 70-80 years old. Our results demonstrate a parallelism between generation of the ROS and RNS induced by the age. A significant increase of ROS production was observed from 40 years old (age groups III, IV, V and VI while for RNS this increase was observed only from 50 years old (groups IV, V and VI). These data suggest an increase of oxidizing species generation (ROS/RNS) related to age. The increased generation of ROS (40-49 years old) was induced before the increasing of RNS (50-59 years old) and it may have consequences on inflammation and host defences.
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PMID:Increase of reactive oxygen (ROS) and nitrogen (RNS) species generated by phagocyting granulocytes related to age. 1104 Mar 96

A critical first-line antioxidant defense on the airway epithelial surface against reactive oxygen and nitrogen species (ROS and RNS) is extracellular glutathione peroxidase (eGPx). Little is known about the regulation of eGPx or its role in ROS-mediated lung diseases such as asthma. Here we show that eGPx is increased in the asthmatic airway in comparison to healthy controls. Higher levels of eGPx mRNA in asthmatic airway epithelium verified bronchial epithelial cells as the source for the increased eGPx. The eGPx mRNA in bronchial epithelial cells in vitro increased eightfold after exposure to ROS and glutathione, an essential cofactor for eGPx activity. Alterations in intracellular and extracellular oxidized and reduced glutathione were temporally associated with eGPx induction, further supporting redox mechanisms in gene expression. Overexpression of superoxide dismutase, but not catalase, inhibited induction and identified superoxide as a key intermediary. The eGPx mRNA half-life was not affected by ROS, suggesting a transcriptional mechanism for eGPx regulation. Fusion genes of deletion fragments of the eGPx gene 5' flanking region driving a reporter gene conclusively identified the ROS-responsive region, which contained the consensus DNA binding site for the redox-regulated transcription factor, activator protein 1.
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PMID:Extracellular glutathione peroxidase induction in asthmatic lungs: evidence for redox regulation of expression in human airway epithelial cells. 1114 94

Proteins constitute the major 'working force' for all forms of biological work. Their exact conformation and pattern of folding are tightly connected to their activity and function. Reactive oxygen and nitrogen species (ROS and RNS) are formed during normal metabolism and in higher fluxes under pathological conditions. They cause cellular damage, an important part of which is the oxidation of amino acid residues on proteins, forming protein carbonyls. Other direct modifications of protein side chains, such as o-tyrosine, chloro-, nitrotyrosine, and dityrosine, have been identified. In addition, carbohydrate and lipid derivatives can react with proteins to form adducts that can be analyzed. Protein carbonyl content (PCC) is the most widely used marker of oxidative modification of proteins. There are several methodologies for the quantitation of PCC; in all of them 2,4-dinitrophenyl hydrazine is allowed to react with the protein carbonyls to form the corresponding hydrazone, which can be analyzed optically by radioactive counting or immunohistochemically. Using PCC as a marker, it could be demonstrated that oxidative damage to proteins correlates well with aging and the severity of some diseases. A critical evaluation of PCC and other markers of protein oxidation is presented, together with examples of protein oxidation in diabetes, neurodegenerative diseases, and aging.
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PMID:Human studies related to protein oxidation: protein carbonyl content as a marker of damage. 1119 Dec 80

During intercellular induction of apoptosis, transformed fibroblasts are specifically eliminated by their nontransformed neighbours. This potential control step of oncogenesis is based on a sophisticated system of interdependencies and interactions of reactive oxygen and nitrogen species. Activated nontransformed effector cells release a novel peroxidase and nitric oxide. Superoxide anions generated extracellularly by transformed cells participate in intercellular signalling and also determine transformed cells as selective targets for intercellular induction of apoptosis. The interaction of these molecules results in two major signalling pathways, which are based on HOCl/hydroxyl radicals and on NO/peroxynitrite. In addition, involvement of nitrylchloride seems to be conceivable in an alternative pathway. Hydrogenperoxide plays a central and ambivalent role by fostering the HOCl/hydroxyl radical pathway and by inhibiting the NO/peroxynitrite pathway. The interaction of ROS and RNS during intercellular induction of apoptosis seems to represent a general signalling concept utilized by several natural antitumor systems.
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PMID:Reactive oxygen and nitrogen species: efficient, selective, and interactive signals during intercellular induction of apoptosis. 1120 38

Recent experimental findings suggest that overproduction of reactive oxygen and nitrogen species (ROS/RNS), lowered antioxidant defense and alterations of enzymatic pathways in humans with poorly controlled diabetes mellitus can contribute to endothelial, vascular and neurovascular dysfunction. Over the past decade, there has been substantial interest in oxidative stress and its potential role in diabetogenesis, development of diabetic complications, atherosclerosis and associated cardiovascular disease. Consequences of oxidative stress are damage to DNA, lipids, proteins, disruption in cellular homeostasis and accumulation of damaged molecules. This review summarizes recent knowledge on the pathomechanism of ROS/RNS in vascular oxidative stress and Maillard reactions. Evidence suggests that Maillard reactions act as amplifier of oxidative damage in aging and diabetes. Furthermore, results of experimental observations with antioxidant systems and antioxidant pharmacotherapy in the treatment of diabetes mellitus are discussed. These data indicate that the targeting therapy to specific macromolecules, tissues and organs of diabetics by specific antioxidants or combined drug preparates could become a relevant adjuvant pharmacotherapy with improved glycaemic control, blood pressure control and management of dyslipidemia for the treatment or prevention of progression of micro- and macrovascular diabetic complications. Supplementation with antioxidants as a promising complementary treatment can exert beneficial effects in diabetes. Some antidiabetic drugs may have antioxidant properties independently of their main role on glycaemia control. Therapeutic potential of inhibitors of AGEs formation for delaying of diabetic complications is now intensively studied in several laboratories. Furthermore, for functional outcomes of the intervention with antioxidants is also important development of accurate and sensitive methods for early detection of oxidative damage in diabetes. (Tab. 6, Fig. 3, Ref. 117.)
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PMID:The role of free radicals, oxidative stress and antioxidant systems in diabetic vascular disease. 1121 44

Transient generation of reactive oxygen or nitrogen (ROS/RNS), detected with dihydrodichlorofluoroscein by fluorescence microscopy, occurs within minutes of exposing cells to ionizing radiation. In the 1-10 Gy dose range, the amount of ROS/RNS produced/cell is constant, but the percentage of producing cells increases with dose (20 to 80%). Reversible depolarization of the mitochondrial membrane potential () and decrease in fluorescence of a mitochondria-entrapped dye, calcein, are observed coincidentally. Radiation-induced ROS/RNS, depolarization, and calcein fluorescence decrease are inhibited by the mitochondrial permeability transition inhibitor, cyclosporin A, but not the structural analogue, cyclosporin H. Radiation-stimulated ROS/RNS is also inhibited by overexpressing the Ca(2+)-binding protein, calbindin 28K, or treating cells with an intracellular Ca(2+) chelator. Radiation-induced ROS/RNS is observed in several cell types with the exception of rho(o) cells deficient in mitochondrial electron transport. rho(o) cells show neither radiation-induced ROS/RNS production nor depolarization. We propose that radiation damage in a few mitochondria is transmitted via a reversible, Ca(2+)-dependent mitochondrial permeability transition to adjacent mitochondria with resulting enhanced ROS/RNS generation. Measurements of radiation-induced mitogen-activated protein kinase activity indicate that this sensing/amplification mechanism is necessary for activation of some cytoplasmic signaling pathways by low doses of radiation.
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PMID:Ionizing radiation-induced, mitochondria-dependent generation of reactive oxygen/nitrogen. 1135 2

Oxidative stress is one of the major causes of cellular injury. Various reactive oxygen (ROS) and nitrogen (RNS) species such as superoxide, hydroxyl radical, peroxynitrite, and nitric oxide are involved in the manifestations of different types of organ toxicity and the resultant syndromes, symptoms, or diseases. Hypothermic conditions have been reported to reduce the oxidative stress in various in vitro and in vivo studies. In the present study, we sought to determine the effect of lowered temperatures on oxidative stress-induced cell death in Chinese hamster ovary (CHO) cells. We also investigated the oxidative stress-induced alterations in the expression of anti-apoptotic protein, bcl-2, in CHO cells at lowered temperatures. CHO cells were incubated at four different temperatures of 30, 32, 35, and 37 degrees C (control temperature) from 1 to 4 d. In another set, the cells were incubated with 100 microM hydrogen peroxide (H(2)O(2)) for 30 min before harvesting at different time points. The cells were harvested at 1, 2, 3, and 4 d. Cell survival was significantly higher at 30 degrees C as compared to 37 degrees C over 4 d of incubation. In cells incubated with H(2)O(2), significantly higher cell viability was observed at lower temperatures as compared to the cells incubated at 37 degrees C. The activity of glutathione peroxidase (GSH-Px) also increased significantly at lower temperatures. Lowered temperature also provided a significant increase in the expression of anti-apoptotic protein, bcl-2 after 4 d of incubation. These data suggest that hypothermic conditions lowers the risk of oxidative stress-induced cellular damage and programmed cell death by increasing the activity of GSH-Px and by the induction in the expression of the anti-apoptotic protein, bcl-2.
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PMID:Hypothermia enhances bcl-2 expression and protects against oxidative stress-induced cell death in Chinese hamster ovary cells. 1146 79


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