Search results for "Active oxygen"
showing 10 items of 884 documents
Uncoupling of Endothelial Nitric Oxide Synthase in Cardiovascular Disease and its Pharmacological Reversal
2010
Publisher Summary This chapter discusses the role of oxidative stress in vascular dysfunction and atherogenesis, and strategies for its prevention. Endothelial dysfunction and oxidative stress have been identified as a common denominator of many cardiovascular risk factors. They support pro-inflammatory, prothrombotic, proliferative, and vasoconstrictor mechanisms that are involved in the initiation, progression, and complications of atherosclerosis. The pathophysiologic causes of oxidative stress involve changes in a number of different enzyme systems. Increased production of ROS by uncoupled eNOS is likely to contribute significantly to vascular oxidative stress and endothelial dysfunctio…
Magnesium, Oxidative Stress, and Aging Muscle
2014
Abstract Magnesium (Mg) deficiency, aside from having a negative impact on the energy production pathways required by the mitochondria to generate ATP, also reduces the threshold antioxidant capacity of the aging organism and its resistance to free-radical damage. Mg acts as an antioxidant against free radical damage of the mitochondria. Chronic Mg deficiency results in excessive production of oxygen-derived free radicals and low-grade inflammation. Chronic inflammation and oxidative stress have been identified as pathogenic factors in several age-related conditions. Aging is often associated with Mg inadequacy, muscle loss, and sarcopenia. Although the importance of magnesium as a determin…
Antioxidants in skeletal muscle physiology, a radically different approach.
2015
Regular physical exercise has many health benefits (1). Paradoxically, it is also clear that contracting skeletal muscles generate reactive oxygen species (ROS) and that prolonged and intense exercise can result in oxidative damage to cellular constituents (2-4). Reactive oxygen species production is dependent on the intensity of the exercise with higher amount of ROS generated by strenuous exercise (5, 6). Antioxidants may reduce the adverse effects of exercise-induced ROS (2-4). However, ROS are not only toxic but rather play an important role in cell signalling and in the regulation of gene expression (7, 8) and force production in skeletal muscle (9). Thus, we have recently raised quest…
Senescence and p130/Rbl2: a new beginning to the end.
2009
Senescence is the process of cellular aging dependent on the normal physiological functions of non-immortalized cells. With increasing data being uncovered in this field, the complex molecular web regulating senescence is gradually being unraveled. Recent studies have suggested two main phases of senescence, the triggering of senescence and the maintenance of senescence. Each has been supported by data implying precise roles for DNA methyltransferases, reactive oxygen species and other factors. We will first summarize the data supporting these claims and then highlight the specific role that we hypothesize that p130/Rbl2 plays in the modulation of the senescence process.
Oxidative DNA Damage Profiles in Mammalian Cells
1997
Reactive oxygen species (ROS) are formed inside cells not only under the influence of exogenous agents (visible light, ionizing radiation, and many oxidants such as peroxides or quinones), but also under normal (physiological) conditions as byproducts of oxygen metabolism and other cellular redox reactions (Pryor 1986; Halliwell and Gutteridge 1986; Sies 1986; Clayson et al. 1994). ROS such as hydroxyl radicals and singlet oxygen are a serious threat to the integrity of the cellular genome, since they efficiently react with DNA to generate many types of DNA modifications, at least some of which are pre- mutagenic (Breimer 1990; Halliwell and Aruoma 1991; Epe 1991; Feig et al. 1994). Steady-…
Mitochondrial Oxidative Stress in Diabetes
2014
Abstract Diabetes is a multifactorial disease associated with serious comorbidities. This condition has been related to oxidative stress and, as a consequence, to overproduction of reactive oxygen species (ROS), which are known to be produced by different sources in diabetes. Excessive production of ROS can be harmful, making antioxidant defenses of vital importance. Dietary antioxidants, such as vitamin E or vitamin C, polyphenols and flavonoids have been used to modulate the oxidative stress created in diabetes, producing contradictory results in clinical trials, perhaps as a consequence of the targets selected and/or the design of the studies in question. This chapter considers the proce…
Exercise as an antioxidant: it up-regulates important enzymes for cell adaptations to exercise
2006
Abstract Aims. – To assess the role of the reactive oxygen species (ROS) in cell signalling and in the regulation of gene expression. Methods. – Exercise causes oxidative stress only when exhaustive. Strenuous exercise causes oxidation of glutathione, release of cytosolic enzymes, and other signs of cell damage. We have tested this hypothesis by studying the effect of inhibition of ROS production by allopurinol (an inhibitor of xanthine oxidase, a free radical generating enzyme) on cell signalling pathways in marathon runners and in rats submitted to exhaustive exercise by running on a treadmill. Results. – Exercise caused an activation of NF-κB in lymphocytes from marathon runners which wa…
Oxygen Radical Scavengers
2010
The myocardium can tolerate only relatively short periods of total myocardial ischemia without myocardial cell death. Following short ischemic periods, ischemic damage is reversible by reperfusion. However, with increasing duration and severity of ischemia, the damage inflicted to cardiomyocytes following reperfusion becomes irreversible. The combined pathologic events in the myocardium that follow a critical period of ischemia and leading to either reversible or irreversible damage to both cardiomyocytes and cardiac microvasculature is known as ischemia-reperfusion injury (Goldhaber and Weiss 1992).
Nitroglycerin-Induced Endothelial Dysfunction and Tolerance Involve Adverse Phosphorylation and S -Glutathionylation of Endothelial Nitric Oxide Synt…
2011
Objective— Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS). In the present study, we tested the effects of type 1 angiotensin (AT 1 )-receptor blockade with telmisartan on GTN-induced endothelial dysfunction in particular on eNOS phosphorylation and S -glutathionylation sites and the eNOS cofactor synthesizing enzyme GTP–cyclohydrolase I. Methods and Results— Wistar rats were treated with telmisartan (2.7 or 8 mg/kg per day PO for 10 days) and with GTN (50 mg/kg per d…
Microcirculatory Dysfunction Induced by Cigarette Smoking
2000
This review deals with the deleterious effects of cigarette smoking on the microcirculation, both in terms of morphological (i.e., vessel wall injury, capillary loss) and functional aspects. The latter concerns predominantly changes in tissue perfusion and its regulatory mechanisms (i.e., reactive hyperemia, sequestration of blood cells in the microcirculation). The mechanisms of action of cigarette smoking on the microcirculation include compromised endothelial-dependent vasorelaxation, platelet aggregation, endothelial cell dysfunction, and the activation of circulating leukocytes. Through these mechanisms, cigarette smoking elicits the aggregation and adhesion of leukocytes and/or platel…