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

Administration of HgCl2 at a dose of 5 mg/kg body weight/day for 15 days to male albino rats brought about a marked depression of the scavenging enzymes viz. glutathione peroxidase and glutathione S-transferase, in kidney. There was an adaptive rise in the levels of catalase and no increased lipid peroxidation was observed. The levels of both glutathione and glutathione reductase were decreased, whereas total thiol increased. In the intoxicated rats, Vitamin-E was effective in bringing back glutathione levels to normal. The adaptation in this group of animals is reflected by increased superoxide dismutase activities. Feeding of Vitamin-E alone could cause a depression of the scavenging enzymes like glutathione peroxidase and glutathione S-transferase along with a slight lowering of glutathione levels.
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PMID:Effects of mercuric chloride on several scavenging enzymes in rat kidney and influence of vitamin E supplementation. 649 53

A substantial decrease in liver peroxisomal catalase was found during riboflavin deficiency in rats. This decrease is greater than that found among other hemoproteins and seems to follow decrease in flavin-dependent peroxisomal oxidases. This is not due to a general depression of peroxisomal enzymes, since Cu-dependent urate oxidase activity was not changed. Furthermore, the level of catalase activity as well as flavin-dependent oxidases was restored by riboflavin repletion. These results suggest that hydrogen peroxide, the substrate for catalase produced by several flavoprotein oxidases, induces catalase in mammals as has been indicated for certain bacteria.
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PMID:Correlation of H2O2 production and liver catalase during riboflavin deficiency and repletion in mammals. 666 73

Kidney post-nuclear supernatants from genetically lean and obese mice were subjected to subcellular fractionation by dual centrifugation through sucrose gradients in B XIV zonal rotors. Considerable purification of peroxisomes was achieved which allowed the demonstration of acyl-CoA beta-oxidation enzymes and carnitine acyltransferases in these organelles. Comparison of kidney peroxisome-enriched fractions from obese and lean mice indicated a likely relative depression in beta-oxidation enzymes in the obese animal. Measurement of catalase, acyl-CoA oxidase and carnitine octanoyltransferase in whole homogenate of liver and kidney of obese and lean mice revealed significantly reduced levels (to approximately 2/3) of these peroxisomal enzymes in the kidney of ob/ob mice. In contrast the specific activity of catalase and acyl-CoA oxidase was significantly raised in the liver of obese mice.
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PMID:Reduced levels of peroxisomal enzymes in the kidney of the genetically obese (ob/ob) mouse. Contrast with liver. 667 44

An initial event in gram-negative bacteremia is activation of the complement cascade with production of C5a. C5a, in turn, acts as a chemotactic stimulus for leukocytic aggregation and, in conjunction with bacterial products, stimulates the release of oxygen free radicals from leukocytes. We have hypothesized that these oxygen free radicals (.O2-, superoxide anion; .OH, hydroxyl radical; H2O2, hydrogen peroxide) contribute to the characteristic myocardial dysfunction of endotoxin shock, Isolated canine cardiac sarcoplasmic reticulum (SR) was used as a subcellular determinant of mechanical function. SR was incubated for 20 min at 37 degrees C in the presence of phorbol myristate acetate activated leukocytes (A-L) and calcium uptake and Ca2+-adenosine triphosphatase (ATPase) activities were measured. Activated leukocytes significantly depressed SR Ca2+ uptake rates (C = 1.12 +/- 0.05 mumol CA2+/mg-min; A-L = 0.73 +/- 0.05). The addition of catalase (CAT; 10 micrograms/ml) or superoxide dismutase (SOD: 10 micrograms/ml) plus CAT reversed the inhibition of SR Ca2+ uptake. SOD further depressed SR Ca2+ uptake (+SOD = 0.55 +/0 0.04 mumol Ca2+/mg-min). Mannitol had no effect. SR ATPase activity was inhibited with A-L (C = 1.41 +/- 0.04 mumol Pi/mg-min; A-L = 0.84 +/- 0.09). Neither mannitol, nor SOD nor CAT alone had any effect on the depression of SR ATPase activity. SOD plus CAT reversed the ATPase depression induced by A-L. It is concluded that phorbol myristate acetate activated leukocytes via free radical-mediated mechanisms can directly affect function and activity of the excitation-contraction coupling system of cardiac muscle. Free radical scavengers identified hydrogen peroxide as a major mediator of depressed Ca2+ uptake rates. In conjunction with the superoxide anion, hydrogen peroxide contributes to the depressed ATPase activity.
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PMID:Interaction of oxygen free radicals and cardiac sarcoplasmic reticulum: proposed role in the pathogenesis of endotoxin shock. 685 Oct 3

Duration and intensity of drug action are greatly influenced by the rates of which drugs are biotransformed by the cytochrome P-450-linked monooxygenase systems of the hepatic endoplasmic reticulum. Several interferon-inducing agents (poly rI.rC, tilorone, vaccines, viruses, endotoxin) are shown to markedly depress hepatic P-450 systems when administered to rodents. The interferon (IF) inducers that depress hepatic drug metabolism also modulate certain immune responses; it is therefore not known whether the depression of P-450 is due to IF per se or to the action of IF-inducing agents on one or more components of the immune system. The loss of cytochrome P-450 elicited by IF-inducing agents is accompanied by a perturbation of heme metabolism associated with the dissociation of heme from cytochrome P-450. The agents also cause losses of hepatic catalase and tryptophan 2,3-dioxygenase. These studies predict that viral infections, vaccinations, and treatment with IF-inducing agents will be shown to seriously impair the metabolism of drugs in humans.
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PMID:Effects of interferon-inducing agents on hepatic cytochrome P-450 drug metabolizing systems. 694 Apr 67

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.
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PMID:Radiation-induced inhibition of human lymphocyte blastogenesis: the effect of superoxide dismutase and catalase. 697 18

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)
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PMID:The role of toxic oxygen metabolites in a young model of thermal injury. 747 25

The Na(+)-K+ ATPase activity and SH group content were decreased whereas malondialdehyde (MDA) content was increased upon treating the porcine cardiac sarcolemma with xanthine plus xanthine oxidase, which is known to generate superoxide and other oxyradicals. Superoxide dismutase either alone or in combination with catalase and mannitol fully prevented changes in SH group content but the xanthine plus xanthine oxidase-induced depression in Na(+)-K+ ATPase activity as well as increase in MDA content were prevented partially. The Lineweaver-Burk plot analysis of the data for Na(+)-K+ ATPase activity in the presence of different concentrations of MgATP or Na+ revealed that the xanthine plus xanthine oxidase-induced depression in the enzyme activity was associated with a decrease in Vmax and an increase in Km for MgATP; however, Ka value for Na+ was decreased. Treatment of sarcolemma with H2O2 plus Fe2+, an hydroxyl and other radical generating system, increased MDA content but decreased both Na(+)-K+ ATPase activity and SH group content; mannitol alone or in combination with catalase prevented changes in SH group content fully but the depression in Na(+)-K+ ATPase activity and increase in MDA content were prevented partially. The depression in the enzyme activity by H2O2 plus Fe2+ was associated with a decrease in Vmax and an increase in Km for MgATP. These results indicate that the depressant effect of xanthine plus xanthine oxidase on sarcolemmal Na(+)-K+ ATPase may be due to the formation of superoxide, hydroxyl and other radicals. Furthermore, the oxyradical-induced depression in Na(+)-K+ ATPase may be due to the formation of superoxide, hydroxyl and other radicals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of cardiac sarcolemma Na(+)-K+ ATPase by oxyradical generating systems. 749 43

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.
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PMID:Suppression of natural killer cell activity by granulocytes in patients with aplastic anemia: role of granulocyte colony-stimulating factor. 751 63

The immune system of the spontaneously hypertensive rat is dysfunctional compared with that of normotensive control strains. Previous studies from our laboratory have shown that immunodepression in the spontaneously hypertensive rat was mediated by macrophages. The current study examines the mechanism for the depressed proliferative responses to concanavalin A typically observed by splenic mononuclear cells of spontaneously hypertensive rats. We tested various inhibitors of known macrophage products responsible for suppressing lymphoid function. The nitric oxide synthetase inhibitor NG-monomethyl L-arginine produced dose-dependent derepression of the proliferative responses of splenic mononuclear cells to concanavalin A. In contrast, indomethacin and catalase exhibited only weak derepression of the proliferative responses. Subsequent analysis showed that splenic mononuclear cells from spontaneously hypertensive rats generated greater nitric oxide levels than cells from Wistar-Kyoto rats, and nitric oxide levels were reduced when the inhibitor was added to splenic mononuclear cell cultures from spontaneously hypertensive rats. We further demonstrated that L-arginine is required for the development of the depressed mitogen-induced proliferative responses in these cells. Addition of L-arginine in excess of 10 microM to cultures diminished cell proliferation and increased nitric oxide. Polyclonal antibodies to murine interferon gamma reduced nitric oxide accumulation by approximately 50%, suggesting that interferon gamma is partially responsible for enhancing nitric oxide production in mitogen-stimulated splenic mononuclear cell cultures from spontaneously hypertensive rats. Thus, this study provides evidence that the immune depression observed in the spontaneously hypertensive rat is nitric oxide dependent.
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PMID:Nitric oxide mediates immune dysfunction in the spontaneously hypertensive rat. 767 89


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