Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitogen-induced lymphocyte blastogenesis was measured following X-irradiation (0-4 Gy) in the presence or absence of superoxide dismutase (SOD), under aerobic and anaerobic conditions. There were no significant differences between radiation survival curves under these different conditions, nor did SOD have any radioprotective effect. This demonstrates the lack of oxygen dependence of radiation-induced inhibition of lymphocyte blastogenesis. Following X-irradiation at 2 Gy, neither SOD nor catalase, alone or together, added before or after irradiation, were radioprotective. In comparison to controls, both enzymes depressed lymphocyte proliferation when added at levels as low as 25 microgram catalase or 100 microgram SOD/ml media. When SOD and catalase were added together, the greatest depression of blastogenesis was obtained with increasing levels of SOD relative to increasing levels of catalase, indicating that SOD was largely responsible for this depression. The suppressive effect of administration of SOD (p less than 0.05), catalase (p less than 0.001) and SOD + catalase (p less than 0.001) on lymphocyte division was significantly greater when given prior to X-irradiation. The lack of an oxygen effect and the inability of SOD and catalase to protect human lymphocytes from X-irradiation suggest that 2- and /or H2O2 are not involved in radiation-induced inhibition of lymphocyte blastogenesis.
 ...
PMID:Radiation-induced inhibition of human lymphocyte blastogenesis: the effect of superoxide dismutase and catalase. 697 18

Paraquat is a widely used herbicide which causes lung injury in animals and humans. To determine whether pulmonary endothelial cell function is altered during the course of paraquat lung toxicity, we measured uptake of serotonin in isolated perfused lungs from rats injected i.p. with 25 mg/kg of paraquat dichloride. In 38 control lungs, serotonin uptake was 0.71 +/- 0.02 (S.E.) and was not significantly different in rats studied 4 and 18 hr after paraquat administration. In contrast, uptakes were 0.60 +/- 0.04 (P less than .05) 24 hr after injection of paraquat. At that time, lung histology and endothelial ultrastructure were unremarkable and dry-to-wet-weight ratios of lungs were normal. Forty-eight hours after paraquat administration, when light and electron microscope evidence of edema and inflammation were extensive, serotonin uptake was further decreased (P less than .01). Two weeks after injection of paraquat, when fibrosis was present, based on lung histology and hydroxyproline content, serotonin uptakes had returned to control levels. Administration of superoxide dismutase prolonged survival but did not protect against paraquat-induced depression of serotonin uptake. These results indicate that paraquat causes an early and reversible depression of pulmonary endothelial cell uptake of serotonin which antedates morphological alterations in lung and the endothelial cell and which is not prevented by treatment with exogenous superoxide dismutase. Uptake of serotonin may provide a sensitive and specific index of injury to the pulmonary endothelium.
 ...
PMID:Depression of serotonin uptake by rat lungs exposed to paraquat. 706 88

Exposure of isolated mouse lung macrophages to 40 and 60 per cent oxygen in tissue culture for 48 hours resulted in significant depression of phagocytosis as compared to air-exposed controls. The impairment of phagocytosis was reversed when the cells were reexposed to normoxic conditions for 48 hours. The impairment of phagocytosis occurred despite significant increases in intracellular superoxide dismutase activity, an enzyme felt to play a protective role in oxygen toxicity. Exposure to 40 and 60 per cent oxygen increased the susceptibility of lung macrophages to functional impairment by 95 per cent oxygen, rather than producing tolerance. The precise biologic and clinical significance of these findings will require additional studies in integrated systems. However, these studies show unequivocal lung macrophage injury with moderate hyperoxic exposure.
 ...
PMID:Impairment of phagocytosis by moderate hyperoxia (40 to 60 per cent oxygen) in lung macrophages. 739 68

Lungs accumulate 5-hydroxytryptamine (serotonin, 5-HT) from the perfusate by a sodium-dependent, energy-requiring, saturable process. The rate-limiting step for uptake is the transport of 5-HT and not its subsequent metabolism to 5-hydroxyindoleacetic acid. Autoradiographic studies indicate that the pulmonary endothelium is the cellular site of uptake. The effect of hyperoxia on lung clearance of 5-HT was studied with isolated perfused and ventilated lungs from rats that were previously exposed to hyperoxia. Lungs were perfused with recirculating electrolyte solution and initial [5-HT] of 0.24 microM. The calculated fractional 5-HT clearance (fracion of 5-HT removed in a single pass) ws 0.77 +/- 0.02 (mean +/- SE: n = 44) for control rats. Mean fractional clearance decreased by 20% in rats exposed to 1 atm O2 for 18 hr and 30% after 4 atmospheres absolute (ata) O2 for 1 hr (p < 0.05). The effects of O2 at 4 ata were in part reversed by exposure to air for 3.5 hr and in part prevented by injection of superoxide dismutase (60 nmole/kg body weight). This degree of O2 exposure at either 1 or 4 ata had no effect on lung content of adenine nucleotides or the distribution of 3H-5HT on autoradiography. Rats maintained for 6 weeks on a vitamin E-deficient diet showed an increased effect of hyperoxia on 5-HT clearance and did not show reversal of changes after 24 hr of air breathing. The results indicate that exposure to elevatd po2 results in reversible depression of pulmonary 5-HT clearance that is potentiated by vitamin E deficiency. This suggests alteration of pulmonary endothelial membrane transport properties due to O2 toxicity.
 ...
PMID:Environmental influences on uptake of serotonin and other amines. 740 97

Production of oxygen-free radicals has been proposed as one pathophysiologic mechanism for postburn cardiac contractile dysfunction in adults. To examine this hypothesis in young subjects, we studied the cardiac effects of polyethylene glycol-superoxide dismutase (PEG-SOD) and PEG-catalase (PEG-CAT), each given as 20 U/g of body weight with fluid resuscitation (Parkland formula), after a third-degree burn constituting 33% of the total body surface area in young (6- to 7-day old) guinea pigs (group 3, n = 12). Fluid-treated burns without scavenger therapy (group 2, n = 15) and sham burn controls (group 1, n = 15) were included. Animals were killed 24 hours postburn, and hearts were studied in vitro (Langendorff). Compared with sham burn controls, fluid-treated burns (group 2) had significant cardiac dysfunction as indicated by a lower peak systolic left ventricular (LV) pressure (LVP: 67 +/- 2 vs. 57 +/- 4 mm Hg, p = 0.01, mean +/- SEM), maximal rate of LV pressure development (+dP/dt max: 1169 +/- 45 vs. 988 +/- 45 mm Hg/second, p = 0.01), and fall (-dP/dt max: 1109 +/- 45 vs. 919 +/- 49 mm Hg/second, p = 0.01). In addition, LV function curves calculated for group 2 were shifted downward and to the right of those calculated for sham burn controls in the direction of contractile depression, p = 0.01. PEG-SOD/PEG-CAT treatment in burns did not significantly improve LVP (60 +/- 5 mm Hg), but scavenger therapy improved +/-dP/dt max values (1112 +/- 74 and 988 +/- 98 mm Hg/second, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The role of toxic oxygen metabolites in a young model of thermal injury. 747 25

The actions of NO synthase inhibitors and indomethacin, a cyclooxygenase inhibitor, on the nonadrenergic noncholinergic (NANC) mechanical responses of cat distal colon were studied in vitro using muscle strips orientated in the axis of the longitudinal muscle layer with pelvic nerves attached. Electrical field stimulation (EFS) or pelvic nerve stimulation (PNS) caused inhibition of spontaneous contractions followed by off-contractions. Indomethacin (10-30 microM) caused concentration-dependent reductions in amplitude and duration of EFS- and PNS-evoked off-contractions but not latency. The NO synthase inhibitors, N omega-nitro-L-arginine (L-NNA), N omega-nitro-L-arginine methyl ester (L-NAME) and NG-monomethyl-L-arginine (L-NMMA) (each at 100 microM) significantly reduced latency, amplitude, and duration of off-contractions evoked by EFS and PNS. This inhibition was partially reversed by L-arginine (120 microM) but not by D-arginine. Incubation of colonic strips with alpha-chymotrypsin (2 U/ml) decreased latency, amplitude, and duration of NANC off-contractions. L-NNA reduced amplitude, duration, and latency of off-contractions in preparations pretreated with alpha-chymotrypsin. Hydroquinone (10-30 microM), a generator of superoxide anions, caused significant depression of amplitude, duration, and latency of off-contractions which was completely reversed by superoxide dismutase (200 U/ml). These data suggest that the components of NANC off-contractions evoked by EFS and PNS involve peptides, NO, and prostaglandins.
 ...
PMID:A nitric oxide and prostaglandin-dependent component of NANC off-contractions in cat colon. 750 99

Patients with aplastic anemia were tested for natural killer (NK) activity, and the roles of granulocytes and granulocyte colony-stimulating factor (G-CSF) in the regulation of cytotoxicity were evaluated. Blood lymphocytes showed low or no NK activity against K562 targets. The depression of NK activity was more frequently recorded for patients who were not in remission and those who received G-CSF administration. Granulocytes of aplastic anemia patients with impaired NK activity suppressed the lytic activity of NK cells. By contrast, granulocytes from normal controls and aplastic anemia patients with normal NK activity had no suppressive activity. There was a good correlation between NK activity of lymphocytes and suppressive activity of granulocytes. Blocking of direct contact of suppressor and effector cells by cell chambers abolished suppression of cytotoxicity. NK suppression by granulocytes was resistant to treatment with catalase or superoxide dismutase. In vitro stimulation with G-CSF of granulocytes that naturally had no suppressive activity resulted in development of suppressive function, whereas granulocytes with natural suppressive activity were not further stimulated in vitro by G-CSF to express augmented activity. These results suggest that the presence of suppressor granulocytes in the blood could be one cause of the impaired NK activity in patients with aplastic anemia.
 ...
PMID:Suppression of natural killer cell activity by granulocytes in patients with aplastic anemia: role of granulocyte colony-stimulating factor. 751 63

We studied the action of H2O2 on the exocytosis of glutamate by cerebrocortical synaptosomes. The treatment of synaptosomes with H2O2 (50-150 microM) for a few minutes results in a long-lasting depression of the Ca(2+)-dependent exocytosis of glutamate, induced by KCl or by the K(+)-channel inhibitor 4-aminopyridine. The energy state of synaptosomes, as judged by the level of phosphocreatine and the ATP/ADP ratio, was not affected by H2O2, although a transient decrease was observed after the treatment. H2O2 did not promote peroxidation, as judged by the formation of malondialdehyde. In indo-1-loaded synaptosomes, the treatment with H2O2 did not modify significantly the KCl-induced increase of [Ca2+]i. H2O2 inhibited exocytosis also when the latter was induced by increasing [Ca2+]i with the Ca2+ ionophore ionomycin. The effects of H2O2 were unchanged in the presence of superoxide dismutase and the presence of the Fe3+ chelator deferoxamine. These results appear to indicate that H2O2, apparently without damaging the synaptosomes, induces a long-lasting inhibition of the exocytosis of glutamate by acting directly on the exocytotic process.
 ...
PMID:Hydrogen peroxide induces a long-lasting inhibition of the Ca(2+)-dependent glutamate release in cerebrocortical synaptosomes without interfering with cytosolic Ca2+. 776 35

Sevoflurane is well known to cause depression of cardiovascular function, but detailed information on its actions on the contractility and reactivity of blood vessels is lacking. We have assessed therefore the direct effect of this anaesthetic on the functional reactivity of isolated rabbit mesenteric artery ring preparations. We found that contractions of endothelium intact rings induced by noradrenaline and phenylephrine were significantly attenuated by 4% sevoflurane; the observation that the maximal tension generation decreased without a significant reduction in pD2 is consistent with the view that receptor dysfunction was not involved. The effect of sevoflurane was not affected by NG-monomethyl-L-arginine. Sevoflurane 4% also produced attenuation of noradrenaline-induced contractions of endothelium denuded ring preparations. The contractions of endothelium denuded ring preparations produced by noradrenaline in Ca(2+)-free media in the presence of K+ were not affected by 4% sevoflurane, but sevoflurane depressed external Ca(2+)-dependent contractions. When vasodilators (acetylcholine and nitroglycerin) were added to the bathing media in the presence of 2% sevoflurane, the endothelium-dependent relaxation produced by acetylcholine, but not the endothelium-independent relaxation produced by nitroglycerin, was attenuated; superoxide dismutase inhibited the effect of sevoflurane on endothelium-dependent relaxation. These results are consistent with the view that sevoflurane inhibits alpha adrenoceptor-mediated contractions of isolated rabbit mesenteric artery ring preparations; this effect may be caused by reduced Ca2+ influx, as estimated from the effect on external Ca(2+)-dependent contractions, but is unlikely to be caused by reduced Ca2+ release from the sarcoplasmic reticulum of vascular smooth muscle, as estimated from noradrenaline-induced contractions in Ca(2+)-free bathing media.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of sevoflurane on the vascular reactivity of rabbit mesenteric artery. 777 35

We investigated the effects 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 enzymatic activity [superoxide dismutase (SOD), catalase, 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 to four groups: group I (sham), 4 hrs duration; group II, 4 hr of shock; group III, 2 hr of shock, followed by reinfusion for 2 hr; and group IV, as in group III, but pretreated with SOD and catalase. Hemorrhagic shock was produced by withdrawing 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; and cardiac MDA, Mn-SOD, and CuZn-SOD increased, while catalase activity decreased during shock. Following reinfusion after 2 hr of shock, hemodynamic parameters and plasma lactate tended to return toward control values. Plasma CK and CK-MB, PMNL-CL and cardiac MDA, total SOD, Mn- and CuZn-SOD increased further, while LV-CL and GSH-Px decreased. In spite of the increased antioxidant reserve, oxidative damage was noted. Pretreatment with SOD and catalase attenuated the deleterious effects of shock and reinfusion on the cardiovascular function, plasma CK, CK-MB, and lactate, PMNL-CL, cardiac MDA and SOD, and LV-CL. Protection was incomplete for cardiovascular function and plasma CK and CK-MB. These results suggest that oxyradicals (O2-, H2O2) may be partly involved in the deterioration of cardiovascular function and cellular injury during hemorrhagic shock and reinfusion.
 ...
PMID:Role of oxyradicals in cardiovascular depression and cellular injury in hemorrhagic shock and reinfusion: effect of SOD and catalase. 783 24


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>