Sources of Free Radicals

McCord, Joe M.; Omar, Bassam

doi:10.1177/0748233793009001-204

Cited by 40 publications

(32 citation statements)

References 95 publications

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“…The cytochromes present in the cell usually reoxidize the ubisemiquinones generated in these reductions; however, ubisemiquinones may also interact with cytochromes to generate 02---The autooxidation of reduced flavoprotein by dehydrogenase is another source of O2-in mitochondria. To protect the cellular integrity from damage by 02-, mitochondria possess an abundant supply of superoxide dismutase (SOD) and vitamin E. These antioxidants function as chain terminators of lipid peroxidation (15). In addition, cytochrome oxidase is also abundant in mitochondria to negate oxygen radical-induced lung injury.…”

Section: Mitochondriamentioning

confidence: 99%

“…In oxygen-deprived and -disrupted tissues, the oxidation of-SH groups or proteolysis by Ca2+-stimulated protease converts the xanthine dehydrogenase to xanthine oxidase. In hypoxia, the oxidation of xanthine and hypoxanthine by xanthine oxidase results in the generation of 02-, which leads to cell injury (8,14,15 (16)(17)(18). The activation of phagocytes triggers a respiratory burst, which is characterized by an increase in oxygen uptake, glucose metabolism, and utilization of NADPH.…”

Section: Eaizymesmentioning

confidence: 99%

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The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

Vallyathan¹,

Shi²

1997

Environmental Health Perspectives

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Oxygen free radicals and their metabolites, collectively described as reactive oxygen species (ROS), have been implicated in the pathogenesis of many diseases. The pulmonary system is particularly vulnerable to ROS-induced injury because of its continuous exposure to toxic pollutants from a wide variety of sources in the ambient air. Additionally, lungs are exposed systemically to ROS generated from xenobiotic compounds and endogenous sources. This review describes the sources of endogenous and exogenous ROS generation in the lung. Special emphasis is given to major sources of ROS in occupational and environmental exposures to asbestos, crystalline silica, coal, chromium, herbicides, bleomycin, and cigarette smoke. ROS-induced lung injury at different target levels may contribute to similar patterns of cell injury and alterations at the molecular level by initiation, propagation, and autocatalytic chain reactions. Intracellular signalling, activation and inactivation of enzymes, stimulation, secretion, and release of proinflammatory cytokines, chemokines, and nuclear factor activation and alterations are also common events. Understanding the interactions of these intricate mechanistic events is important in the prevention and amelioration of lung injury that results from acute and chronic exposures to toxins in ambient air. Environ Health Perspect 1 05(Suppl 1 :1 65-177 (1997)

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Section: Mitochondriamentioning

confidence: 99%

Section: Eaizymesmentioning

confidence: 99%

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

Vallyathan¹,

Shi²

1997

Environmental Health Perspectives

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“…O2-~ formation has given rise to the idea that this free radical is a major reactant in oxygen toxicity (14). While the experimental evidence supporting the O2-.…”

Section: Oxygen Toxicitymentioning

confidence: 99%

Aging and oxygen toxicity: Relation to changes in melatonin

Reíter

1997

AGE

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Melatonin (N-acetyl-5-methoxytryptamine) is a chemical mediator produced in the pineal gland and other sites in the body. The melatonin found in the blood is derived almost exclusively from the pineal gland. Since the pineal synthesizes melatonin primarily at night, blood levels of the indole are also higher at night (5-15 fold) than during the day. Some individuals on a nightly basis produce twice as much melatonin as others of the same age. Throughout life, the melatonin rhythm gradually wanes such that, in advanced age, melatonin production is usually at a minimum. Melatonin was recently found to be a free radical scavenger and antioxidant. It has been shown, in the experimental setting, to protect against both free radical induced DNA damage and oxidative stress-mediated lipid peroxidation. Pharmacologically, melatonin has been shown to reduce oxidative damage caused by such toxins as the chemical carcinogen safrole, carbon tetrachloride, paraquat, bacterial lipopolysaccharide, kainic acid, 8-aminolevulinic and amyloid 13 peptide of AIzheimer's disease as well as a model of Parkinson's disease involving the drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Additionally, the oxidative damage caused by agents such as ionizing radiation and excessive exercise is reduced by melatonin. Since free radical-induced molecular injury may play a significant role in aging, melatonin's ability to protect against it suggests a potential function of melatonin in deferring aging and agerelated, free radical-based diseases. Besides its ability to abate oxidative damage, other beneficial features of melatonin may be important in combating the signs of aging; these include melatonin's immune-stimulating function, its sleep-promoting ability, its function as an anti-viral agent, and general protective actions at the cellular level. Definitive tests of the specific functions of physiological levels of melatonin in processes of aging are currently being conducted.

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“…DM is a major cause for the expression of inflammatory markers, which not only exert direct harm on the cardiovascular system, but also potentiate the negative effects of other cardiovascular risk factors. Hyperglycemia in diabetic patients results in increased intracellular glucose which triggers several pro-inflammatory reactions causing the production of highly toxic oxygen-derived free radicals [33]. Potentiation of NADPH oxidases, endothelial nitric oxide synthase uncoupling, and protein kinase C signaling have been postulated to increase production of vascular superoxide leading to endothelial dysfunction in diabetic patients [34].…”

Section: Diabetes and Inflammation/oxidative Stressmentioning

confidence: 99%

Diabetes Mellitus and the Cardiovascular System

Kolakalapudi¹,

Omar²

2015

J Endocrinol Metab

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Diabetes mellitus (DM) is an epidemic which affects close to 100 million patients worldwide; the majority being type 2 diabetes mellitus. The rising incidence has resulted in a proportional increase in the frequency of cardiovascular disease attributable to DM, as revealed by various population-based studies. Over the past 50 years, DM has been shown to be an important and independent risk factor in the development of a variety of cardiac conditions, especially vascular disease, primarily through accelerated atherosclerosis. Diabetic neuropathy is a serious complication of DM, which leads to the impairment of cardiovascular autonomic control. Diabetic cardiac autonomic neuropathy results in heart rate abnormalities, exercise intolerance, orthostatic blood pressure abnormalities, QT interval prolongation, silent ischemia and diabetic cardiomyopathy, all of which lead to increased morbidity and mortality related to diabetes. This conditions remains difficult to diagnose and treat, requiring a multifaceted approach. Inflammation appears to play a central role in accelerating many of the injurious effects of DM on the cardiovascular system. Expression of specific inflammatory markers has been directly linked to some of the known harmful effects of DM on the cardiovascular system, in addition to indirectly potentiating the deleterious effects of other major cardiovascular disease risk factors. Hyperglycemia results in increased intracellular glucose which triggers several pro-inflammatory reactions leading to the production of harmful free radicals and the formation of advanced glycation end products. These have been linked to the development of diabetic atherogenic dyslipidemia, in addition to glycation and loss of the protective effect of high density lipoproteins in diabetic subjects, thereby worsening the atherosclerotic burden in DM. Addressing hyperglycemia, therefore, is only one of many vital components in the treatment of diabetes. Traditional risk factors for heart disease and stroke tend to be further potentiated by the presence of DM, however, even after adequate control of hyperglycemia. Clinical evidence and major clinical guidelines address this conundrum by pointing out unmet needs of adequate cardiovascular protection, and call for aggressive control of risk factors in the diabetic population.

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Sources of Free Radicals

Cited by 40 publications

References 95 publications

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

Aging and oxygen toxicity: Relation to changes in melatonin

Diabetes Mellitus and the Cardiovascular System

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