UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive oxygen species may be involved in a broad pattern of tissue injury in patients on regular hemodialysis therapy and, in fact, increasing evidence suggests that the antioxidative system is compromized in these patients. One factor contributing to this reduction of antioxidative capacity is selenium deficiency. The present investigation was undertaken to further define the extent and type of impairment of the oxygen radical scavenger system in chronic hemodialysis patients and to evaluate the impact of selenium supplementation. Twelve non-wasted patients (6 male, 6 female, mean age of 58 years) on chronic hemodialysis for a minimum of 5 months (mean 46 months) were supplemented intravenously with 400 mg selenium (as sodium selenite) thrice weekly after each hemodialysis session over 8 weeks. Blood samples were taken before the start, at intervals of 2 weeks during, and 4 weeks after termination of supplementation. Concentrations were evaluated of selenium and alpha-tocopherol in plasma and erythrocytes, of retinol and ascorbic acid in plasma, of glutathione and the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and, catalase (CAT) in erythrocytes. Lipid peroxidation endproducts were measured as malondialdehyde (MDA) in plasma. In patients on hemodialysis multiple alterations of the antioxidative system were present and the concentrations of selenium in plasma, of glutathione and the activity of GSH-Px in erythrocytes were profoundly decreased (p < 0.001). Selenium supplementation improved the selenium status of the patients, as indicated by an increase in selenium concentrations in plasma and erythrocytes and erythrocyte GSH-Px activity. Improvement in antioxidative capacity was further documented by an increase in alpha-tocopherol in erythrocytes. Plasma MDA showed a transient decrease after 6 weeks and increased activities of SOD and CAT were dampened. No effect was seen on plasma concentrations of ascorbic acid, a-tocopherol and retinol. We conclude that patients on chronic hemodialysis therapy manifest a profound depression in antioxidative potential and a selenium deficiency. Selenium supplementation improves the oxygen radical scavenger system and increases selenium concentrations in plasma and erythrocytes and the activity of selenium dependent glutathione peroxidase. Thus, selenium should also be considered for micronutrient supplementation in patients on chronic hemodialysis therapy.
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PMID:Antioxidant status in patients on chronic hemodialysis therapy: impact of parenteral selenium supplementation. 931 Nov 3

The present study focuses on reversible mitochondrial ultrastructural alterations in myocardial myocytes that correspond or accompany reversible metabolic depression observed after oxygen radical exposure. The myocytic mitochondrial membranes and matrix of isolated Langendorff-perfused rat hearts were examined by semiquantitative morphometry using the electron micrograph as unit. The hearts were exposed to either standard perfusion (group A), 10 min of oxygen radicals together with superoxide dismutase and catalase followed by 35 min of recovery (group B), 10 min of oxygen radicals alone (group C), or 10 min of oxygen radicals followed by 35 min of recovery (group D). Mitochondrial ultrastructural alterations were detected in only a few micrographs in groups A and B. The frequency of micrographs with mitochondrial ultrastructural alterations was 69% in group C and 62% in group D. In the group exposed to 10 min of oxygen radicals without recovery (group C) condensed pentalaminar membranous profiles arranged in parallel, interpreted to be closely adhering cristae, were detected in the intracristal compartment of myocytic mitochondria in 50% of the micrographs. The cristal adhesions were associated with other mitochondrial ultrastructural changes. Cristal adhesions were not present in group A or B, and were rarely found in the group exposed to 10 min of oxygen radicals followed by 35 min of recovery (group D). Thus, the cristal adhesions appear to be reversible alterations caused by exposure to oxygen radicals.
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PMID:Reversible ultrastructural alterations in the myocytic mitochondria of isolated rat hearts induced by oxygen radicals. 918 26

Incubation of primary cultures of rat hepatocytes with K2CR2O7 and deferoxamine (DFO), an iron chelator, resulted in a marked decrease in cellular levels of DNA single-strand breaks caused by K2Cr2O7. Cellular treatment with DFO also suppressed both dichromate-induced cytotoxicity--evaluated by the leakage of lactate dehydrogenase, and lipid peroxidation--as monitored by malondialdehyde formation. In addition, treatment with DFO attenuated the suppression of the levels of vitamin E and C as well as the inhibition of alkaline phosphatase and glutathione peroxidase activity attributed to K2Cr2O7. However, DFO had no influence on the cellular level of glutathione or the activity of glutathione reductase and superoxide dismutase suppressed by dichromate. Under the same experimental conditions, cellular uptake and distribution of chromium were not affected by DFO. These results indicate that DFO protects cells from chromium (VI)-induced DNA strand breaks, cytotoxicity, lipid peroxidation, vitamin E and C depression, and glutathione peroxidase inhibition The role of antioxidants in chromium (VI)-induced cytotoxicity, DNA breaks, and lipid peroxidation is discussed.
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PMID:Protective effect of deferoxamine on chromium (VI)-induced DNA single-strand breaks, cytotoxicity, and lipid peroxidation in primary cultures of rat hepatocytes. 919 15

Microperfusion of scala tympani with the NO donors, sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP), produced marked depression of the compound action potential (CAP) and cochlear microphonic (CM) together with severe and widespread morphological damage to hair cells and supporting cells in the organ of Corti. In addition, direct perfusion of N-methyl-D-aspartate (NMDA) into scala tympani, which probably induces excess stimulation of NMDA receptors within the cochlea and which is known to lead to the release of NO, was found to elicit similar electrophysiological and structural lesions in the cochlea. Pre-perfusion of scala tympani with L-methyl arginine (L-MA), which inhibits the release of NO, or superoxide dismutase (SOD), an O2-scavenger, conferred marked protection upon the cochlea from the lesions caused by NO donors. These observations indicate that enhanced NO production is likely to be an important factor responsible for pathological insult of the cochlea. The possibility is discussed that this factor is involved in the chain of events leading to hearing loss caused by bacterial meningitis. Such hearing loss is a major sequela of bacterial meningitis in children.
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PMID:Possible involvement of nitric oxide in the sensorineural hearing loss of bacterial meningitis. 919 17

The effects of different doses of insulin (INS) (0.4 or 4.0 IU/kg body mass, i.p., for 3 hr) and 6-hydroxydopamine (6-HDA) (100 mg/kg., i.p.) on the activities of antioxidant enzymes--copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), catalase (CAT) and catecholamine degrading enzyme monoamine oxidase (MAO-A)--in the rat interscapular brown adipose tissue (IBAT) were studied. In vivo 6-HDA administration, which induces the destruction of sympathetic nerves, markedly reduced IBAT CuZnSOD activity but did not change MnSOD and CAT activities. However, the low dose of INS, which did not induce hypoglycemia, significantly increased the activity of both IBAT mitochondrial enzymes (MnSOD and MAO-A) of control rats. This INS effect on MnSOD was abolished by 6-HDA. On the contrary, CuZnSOD activity was markedly reduced under the influence of INS in both control and 6-HDA-treated rats, whereas for the maintenance of the control level of this enzyme activity, the intact sympathetic nervous system (SNS) is necessary. INS, independent of the dose applied, did not affect CAT activity in control rats, whereas only low INS dose increased the activity of this enzyme in 6-HDA-treated rats. The results indicate that the stimulatory effect of INS on the IBAT mitochondrial enzymes studied is dose dependent and in the case of MnSOD is mediated by SNS. However, the depression in the activity of CuZnSOD is independent of the above-mentioned factors.
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PMID:Activities of antioxidant enzymes and monoamine oxidase-A in the rat interscapular brown adipose tissue: effects of insulin and 6-hydroxydopamine. 921 19

In isolated canine middle cerebral arteries contracted with prostaglandin F2 alpha, transmural electrical stimulation (TES), nicotine, and substance P produced relaxations. Transmural electrical stimulation- and nicotine-induced endothelium-independent responses are mediated by nitric oxide (NO) liberated from perivascular nerve, whereas substance P-induced relaxations are mediated by endothelium-derived NO. These responses were attenuated by replacement of 95% O2 and 5% CO2 gas (about 550 mm Hg of partial O2 pressure) with 95% N2 and 5% CO2 gas (about 40 mm Hg); inhibition of the response to TES was stabilized 30 minutes later. Reoxygenation partially reversed the response. Relaxations caused by exogenous NO were not influenced by hypoxia. Inhibition by hypoxia of the response to TES was not affected by superoxide dismutase. However, the inhibitory effect was prevented by amiloride and dimethyl-amiloride, Na(+)-H+ exchange inhibitors, or acidosis caused by the addition of HCl. The inhibition by hypoxia was reversed by amiloride. It is concluded that depression by hypoxia of the response mediated by endogenous NO is associated with impaired membrane function caused by restoration of normal intracellular pH by Na(+)-H+ exchanger.
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PMID:Hypoxia-induced inhibition of the response to nitroxidergic nerve stimulation in canine cerebral arteries. 927 Apr 98

Acidosis during exercise has long been associated with skeletal muscle fatigue. Recent evidence also has linked reactive oxygen species (ROS) with fatigue in skeletal muscle, including the diaphragm. We hypothesized that acidosis (designed to mimic blood pH during maximal exercise) would worsen ROS-induced depression of diaphragm contractility. The xanthine oxidase (XO) reaction in solution (0.01 U/ml) allows direct assessment of the effects of oxidant stress by ROS. Costal diaphragm fiber bundles from 24 Sprague-Dawley rats (200-250 g) were divided into four treatment groups: 1) pH 7.4, no XO (H); 2) pH 7.4 + XO (HXO); 3) pH 7.0, no XO (L); and 4) pH 7.0 + XO (LXO). Baseline twitch mechanics and force-frequency relationships (Pre) were determined in control Krebs solution (pH 7.4, no XO) before treatment. Treatment solutions were introduced, and the diaphragm underwent 2 min of contractions at 25 Hz (250 ms) at a rate of 1/s. After 10 min of recovery, the control solution was reintroduced into the bath and postcontractile function (Post) was measured. Significant reductions in twitch tension and low-frequency tetanic tension were greater in HXO and LXO compared with H, without an effect on maximal tetanic tension. One-half relaxation time was prolonged only by the combination of acidosis and oxidative stress. Addition of superoxide dismutase (50 U/ml) worsened and catalase (1,800 U/ml) attenuated XO-induced depression of diaphragm contractility. We concluded that XO induced a reduction of low-frequency tension in the fatigued diaphragm, which was mediated directly or indirectly through hydrogen peroxide and was exacerbated to a modest extent with acidosis.
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PMID:Effect of oxidative stress and acidosis on diaphragm contractile function. 927 48

We investigated the effect of hemorrhagic shock and reinfusion on the cardiac function and contractility, plasma CK and CK-MB activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL), cardiac chemiluminescence (LV-CL), antioxidant enzyme activity [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX)] and malondialdehyde (MDA) concentration in anesthetized dogs to determine the role of oxyradicals in cardiac depression and cellular injury in hemorrhagic shock and reinfusion. The dogs were assigned into three groups: I (sham), 4 h duration; II (S + R), 2 h of shock followed by reinfusion for 2 h; III (SOD + S + R), as II but pretreated with PEG-SOD. Hemorrhagic shock was produced by withdrawal of blood to maintain the mean arterial pressure at 50 +/- 5 mm Hg. Cardiac function and contractility were depressed during hemorrhagic shock. Plasma CK, CK-MB and lactate increased during shock. Following reinfusion after 2 h of shock hemodynamic parameters and plasma lactate tended to return towards control values. Plasma CK and CK-MB, PMNL-CL and cardiac MDA, total-, Mn- and CuZn-SOD activity increased while LV-CL decreased. In spite of the increase in the antioxidant reserve, there was oxidative damage. Pretreatment with SOD attenuated the deleterious effects of shock and reinfusion on the cardiovascular function, plasma CK, and CK-MB, PMNL-CL, cardiac MDA, SOD, and LV-CL. Protection was incomplete for cardiovascular function and plasma CK and CK-MB. These results suggest that oxyradicals may partly be involved in the deterioration of cardiovascular function and cellular injury during hemorrhagic shock and reinfusion.
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PMID:Cardiac depression and cellular injury in hemorrhagic shock and reinfusion: role of free radicals. 940 75

Pneumotoxic effects of the tri-n-butyl phosphate (TBP) are investigated on rats using biological markers in bronchoalveolar lavage fluid (BALF) and studying key antioxidant enzymes in lung homogenate. Each animal from the experimental group received intratracheally 5 microliters TBP (20% v/v in n-dodecane). Six rats from the control and treated groups are sacrificed on post-treatment days 1, 3, 7, 14, and 28. The lactate dehydrogenase activity, the total protein content and the total cell number in BALF are increased mainly on day 1 after the treatment. The activities of superoxide dismutase and catalase are decreased to day 7 and those of glutathione peroxidase and glutathione reductase on day 1 only. The malondialdehyde content is elevated to day 14. It is concluded that TBP causes moderate toxic injury of the lung parenchyma. The depression of the key antioxidant enzymes and the elevated lipid peroxidation are probably important mechanisms of the lung damage.
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PMID:Antioxidant defense mechanisms in the lung toxicity of tri-n-butyl phosphate. 940 24

Reactive free radical species appear to be involved in the ischemic injury of cardiac muscle, although the mechanisms by which oxygen-derived free radicals affect the heart cell function are not known. In the present study, cultured ventricular myocytes were exposed to an exogenous oxygen radical generating system. The myocyte-enriched, primary cultures were prepared from ventricles of new-born rat heart and exposed to a xanthine/xanthine oxidase (X+XO) system. The transmembrane potentials were recorded with glass microelectrodes. Cell contractions were monitored photometrically. The release of lactate dehydrogenase (LDH) in the medium was analysed. Quantitative measurement and the time course of the radical generation were performed by the electron paramagnetic resonance (EPR) spin trapping technique with the spin trap 5,5-dimethyl-1-pyroline-N-oxide (DMPO). We verified that X and XO alone had no significant functional and biochemical effects. The X+XO system produced a rapid decrease in the action potential amplitude. This effect was accompanied by a strong decrease in contractility and spontaneous rate. The time course of these functional defects were correlated with a progressive efflux of LDH from the cardiomyocytes. Prolonging the exposure to the X+XO system provoked the cessation of the spontaneous beatings and the progressive loss of the resting diastolic potential, together with a near total release of the cellular LDH. The LDH release and the functional depression were both efficiently prevented by catalase. On the contrary, superoxide dismutase (SOD) slowed down but did not protect against the functional and biochemical effects of the free radicals. In comparison, the EPR spectra obtained indicated that the X+XO system was associated with an important generation of superoxide anions but also with a small hydroxyl production. SOD scavenged the superoxide but a small .OH production persisted. Catalase (CAT) did not modify the superoxide generation but decreased the hydroxyl adduct formation. These results suggest that, although the generation of superoxide anions by the X+XO system was higher than the hydroxyl production, the functional injury and enzyme leakage seemed mainly mediated through a hydrogen peroxide-hydroxyl radical pathway. Cultured ventricular myocytes can be thus used as a valuable model to investigate the cellular mechanism of oxidant-induced damage in the heart.
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PMID:Correlation between direct ESR spectroscopic measurements and electromechanical and biochemical assessments of exogenous free radical injury in isolated rat cardiac myocytes. 943 21

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