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)

Yearling steers were treated with ACTH to determine the effect of increased plasma cortisol concentration on bovine lymphocyte and polymorphonuclear leukocyte (PMN) function. The administration of ACTH caused a significant (P less than 0.01) increase in serum cortisol concentration and depression of lymphocyte blastogenesis in response to phytohemagglutinin and concanavalin A. The response to pokeweed mitogen was also depressed, but not significantly. Random migration by PMN was significantly enhanced by ACTH treatment, but there was no effect on ingestion of Staphylococcus aureus, nitroblue tetrazolium reduction, or antibody-dependent cell-mediated cytotoxicity by PMN. The iodination reaction, which evaluates the activity of the myeloperoxidase-hydrogen peroxide-halide antibacterial system of the PMN, was significantly impaired after ACTH treatment. These data indicate that specific parameters of lymphocyte and neutrophil function were impaired directly or indirectly by elevated in vivo concentrations of plasma cortisol.
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PMID:Effects of ACTH administration on bovine polymorphonuclear leukocyte function and lymphocyte blastogenesis. 628 May 26

The roles of microfilaments and microtubules in the hepatocellular uptake, translocation, and biliary excretion of horseradish peroxidase and [14C]sodium taurocholate were investigated using the microfilament inhibitor cytochalasin D and the microtubule inhibitor colchicine. In separate studies, horseradish peroxidase and [14C]taurocholate were injected separately as a bolus into rat portal veins after treatment with cytochalasin D or colchicine, and bile was collected and analyzed for the presence of horseradish peroxidase and [14C]taurocholate. Cytochalasin D treatment depressed bile flow by approximately 50% and decreased the biliary secretion of [14C]taurocholate in direct proportion to bile flow. Horseradish peroxidase secretion into bile was unaffected, and total biliary protein secretion was decreased only slightly. Because of the depression of bile secretion, concentrations in bile of horseradish peroxidase and total biliary protein increased significantly. Consistent with reported observations of cytochalasin D, decreases in microfilaments and dilated bile canaliculi were observed by electron microscopy; however, the vesicular transport of horseradish peroxidase as observed using electron microscopy cytochemistry appeared to be normal and unaffected by cytochalasin D treatment. Colchicine, in contrast, had minimal effect on bile flow and did not diminish the biliary secretion of [14C]taurocholate. Colchicine inhibited both the total amount of horseradish peroxidase secreted into bile as well as the rate of its secretion in comparison with control and cytochalasin D-treated animals. Cellular morphology was consistent with published observations for colchicine, which included a marked decrease in microtubules. In addition, after electron microscopy cytochemistry there was a paucity of horseradish peroxidase-containing vesicles within the hepatocytes, suggesting that colchicine interfered with the vesicular transport of horseradish peroxidase. Collectively, the data suggest that (a) the mechanism used by hepatocytes for the secretion of bile acids is independent of the vesicular transport of biliary proteins and is dependent upon intact microfilaments and (b) such vesicular transport of protein into bile requires an intact and functioning microtubular network.
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PMID:Effects of cytochalasin D and colchicine on the uptake, translocation, and biliary secretion of horseradish peroxidase and [14C]sodium taurocholate in the rat. 668 8

Dose-dependent increases in alkaline phosphatase and acid phosphatase activities, decreases in myeloperoxidase activity of neutrophils and depression of lymphocyte glycerophosphate dehydrogenase and succinate dehydrogenase activities were discovered in rat nephropathy induced by mercuric chloride at doses of 0.1-1.0 mg/kg. These changes manifest the intensity of the oxidation-reduction process, the reduction of Kreb's cycle and alpha-glycerophosphatic shunt, the damage by peroxidation and the increase in catabolic processes. The morphometric data of nephron structure reflected the functional cell stress and they were compared with leucocyte enzyme status changes.
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PMID:Some aspects of testing drugs for nephrotoxicity in rats. 677 35

Physiological investigations have indicated that the ventrolateral surface of the medulla oblongata is involved in the chemical drive to respiration. In this investigation, light and electron microscopic investigations of the 3 chemosensitive regions reveal the following. (1) Evaginations of the ventral surface abut the overlying pia mater thereby delimiting discrete compartments; invaginations of the surface delimit wide cisternae lined with basement membrane. Neuronal elements with numerous synapses, were found scattered among astrocytic processes of the marginal glia in intermediate and caudal chemosensitive areas Microvasculature are conspicuously absent from the marginal glia. Intramedullary vessels are surrounded by perivascular spaces and the endothelium shows zonulae occludentes at cell junctions. (2) Horseradish peroxidase (HRP) applied to the ventral surface diffused throughout the interstitial and perivascular compartments, into synaptic clefts and neuronal soma. Diffusion of HRP into blood vessels was blocked at zonulae occludentes. Following intravenous injection of HRP, no reaction product was found outside cerebral vasculature in chemosensitive areas. (3) In spontaneously breathing cats, 2% procaine applied to the caudal chemosensitive area resulted in respiratory depression which began with the second breath. It is proposed, that substances which stimulate or depress respiration, when applied to the ventral medullary surface, produce their effects on superficial neurons located in the intermediate and caudal chemosensitive areas after diffusion through interstitial spaces.
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PMID:Morphological observations on superficial medullary CO2--chemosensitive areas. 681 54

Polymorphonuclear leukocyte function and lymphocyte blastogenesis in response to mitogens were evaluated in castrated male cattle after the repeated administration of estradiol or progesterone. Polymorphonuclear leukocyte function was evaluated with the following five parameters: (i) random migration under agarose, (ii) ingestion of 125I-labeled Staphylococcus aureus, (iii) nitroblue tetrazolium reduction, (iv) iodination, and (v) antibody-dependent cell-mediated cytotoxicity. The administration of high dosages of estradiol cypionate produced no measurable effect on the total or differential leukocyte count, neutrophil function, lymphocyte blastogenesis, or blood cortisol levels. The administration of high dosages of progesterone caused a significant enhancement of random migration by neutrophils and a depression of the activity of the myeloperoxidase-H2O2-halide antibacterial system (iodination) of the neutrophil. Progesterone administration did not cause a measurable effect on the lymphocyte blastogenic response to mitogens or the ability of polymorphonuclear leukocytes to ingest S. aureus, reduce nitroblue tetrazolium, or mediate antibody-dependent cell-mediated cytotoxicity. Progesterone did not cause a change in blood cortisol concentrations; therefore, the observed effects on polymorphonuclear leukocyte function were not due to alterations in blood cortisol concentrations. Impairment of the iodination reaction indicates that high dosages of progesterone interfere with an important bactericidal mechanism of the neutrophil.
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PMID:Effect of estradiol and progesterone on lymphocyte and neutrophil functions in steers. 706 28

The present study examined the effect of various unopsonized strains of influenza A virus on release of myeloperoxidase (MPO) and acid phosphatase in polymorphonuclear leukocytes (PMNL). These results were correlated with the effect that these same viruses had on bactericidal activity in PMNL. Several strains of virus inhibited the fusion of azurophil granules with phagosomes containing Staphylococcus aureus. These same strains inhibited the extracellular release of MPO from PMNL (39-59%) and caused depressed killing (42-77%). In contrast, one of the influenza viruses (X-47a) did not inhibit PMNL MPO release or killing. The data indicate a close relationship between the ability of influenza virus to ablate normal intracellular lysosome-phagosome fusion with subsequent depression of bactericidal functions of PMNL.
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PMID:Inhibition of neutrophil lysosome-phagosome fusion associated with influenza virus infection in vitro. Role in depressed bactericidal activity. 708 79

The phospholipid polar head group composition of LM fibroblast membranes was altered by growing the cells in a chemically defined, serum-free medium containing choline, N,N'-dimethylethanolamine, N-monomethylethanolamine, or ethanolamine. The cells incorporated these bases into their membrane phospholipid such that 29-40% of the total plasma membrane phospholipids contained these polar head groups. Alteration of the phospholipid composition correlated with a depression of polystyrene bead phagocytosis by 36, 55 and 85% when the cells had been supplemented with N,N'-dimethylethanolamine, N-monoethylethanolamine, or ethanolamine, respectively. Pinocytotic uptake of horseradish peroxidase was depressed 44, 39, and 32%, respectively. The phagosomal membrane phospholipid composition qualitatively resembled that of the primary plasma membrane from which it was derived. However, enrichment of phosphatidylcholine, and other quantitative differences were noted in the phagosomal membranes as compared to the parent primary plasma membrane. Approx. 50% of the phagosomal membrane's phosphatidylethanolamine was accessible to the chemical labelling reagent trinitrobenzenesulfonate at 4 degrees C. The asymmetric distribution of phosphatidylethanolamine across the phagosomal membrane did not appear to be altered by base analogues except in the case of phagosomes from cells supplemented with ethanolamine. The data were consistent with a nonrandom site for endocytosis with regard to phospholipid composition.
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PMID:Altered phospholipid composition affects endocytosis in cultured LM fibroblasts. 731 90

Antidepressants such as desipramine induce axonal regeneration of brain noradrenergic neurons. This novel action of antidepressants suggests the involvement of degeneration or retraction of brain noradrenergic axons in the pathophysiology of clinical depression. The present study was designed to further confirm this view in an animal model of stress-induced depression. The depression model was produced by exposing rats to prolonged forced walking stress. To see if axonal degeneration of noradrenergic neurons occurred in the depression model, the density of noradrenergic axons in the cerebral cortex was assessed by three different methods, antidromic stimulation technique, retrograde tracing with horseradish peroxidase and immunohistochemical staining with dopamine-beta-hydroxylase antiserum. These methods all assured of degenerative changes of noradrenergic axon terminals in the depression model. Furthermore, it was found that repeated treatments of the depression-model rats with imipramine could cause regeneration of cortical noradrenergic axons. These findings support the view that degeneration or retraction of noradrenergic axons is involved in the pathophysiology of depression.
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PMID:Degeneration of locus coeruleus axons in stress-induced depression model. 753 98

We examined the possible factors that could contribute to the impairment of polymorphonuclear neutrophil (PMN) bactericidal activities in patients with esophageal cancer, based on the discovery that a depression of the intracellular killing (KI) activity, with an elevation of the superoxide anion-producing capacity (SOP), of PMN is associated with the occurrence of infectious complications following surgery for esophageal cancer. KI, SOP, and myeloperoxidase (MPO) activity were measured in 30 patients with esophageal cancer and 33 patients with gastric cancer. Sex, age, and cancer stage were not significantly associated with impaired bactericidal activities; however, malnutrition was significantly correlated with both a depression in KI (r = 0.58, P < 0.001) and an elevation in SOP (r = -.36, P < 0.05) in the patients with esophageal cancer, but not in those with gastric cancer. The incidence of chronic obstructive pulmonary disease (COPD) was significantly higher in the esophageal cancer patients whose SOP was elevated, at 39% versus 0% (P < 0.05). These results suggest that malnutrition and probably also latent infections associated with COPD contribute to the impaired bactericidal activities of PMN in patients with esophageal cancer.
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PMID:Factors related to impaired bactericidal activity in patients with esophageal cancer. 763 20

The primary defence mechanism of myocytes against peroxides and peroxide-derived peroxyl and alkoxyl radicals is the glutathione redox cycle. The purpose of the present study was to increase the turnover rate of this cycle by stimulating the glutathione peroxidase catalysed reaction (2GSH-->GSSG), the glutathione reductase catalysed reaction (GSSG-->2GSH), or both. Neonatal rat heart cell cultures were subjected to a standardized protocol of oxidative stress using 80 mumol.l-1 cumene hydroperoxide (CHPO) for 0-90 min. The consequences of this protocol were described in terms of cellular concentrations of GSH, GSSG, NADPH and ATP, formation of malondialdehyde (MDA), release of GSSG and of ATP catabolites, depression of contraction frequency, cellular calcium overload, and enzyme release. Trolox-C, an analogue of vitamin E, accelerated the glutathione peroxidase reaction leading to lowering of GSH concentration and the GSH/GSSG ratio, less MDA formation, diminished negative chronotropy, delayed calcium overload, and less enzyme release. Glucose was used to accelerate the glutathione reductase reaction by supplying NADPH, leading to higher GSH concentration and a higher GSH/GSSG ratio, less MDA formation, diminished negative chronotropy, unchanged development of calcium overload, and less enzyme release. As a full turn of the glutathione redox cycle involves both the peroxidase and the reductase reactions, the combination of Trolox-C and glucose was superior to either of the two alone: 90 min following addition of CHPO together with Trolox-C and glucose, the GSH concentration and the GSH/GSSG ratio were almost normal, MDA formation was extremely low, calcium overload was markedly delayed, and enzyme release hardly occurred at all. Cells remained beating in the observation period of 30 min. We conclude that the capacity of the glutathione redox cycle to withstand oxidative stress can be increased by stimulation of either the peroxidase reaction or the reductase reaction, and that optimal redox cycling is achieved by stimulation of both reactions.
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PMID:Protection of myocytes against free radical-induced damage by accelerated turnover of the glutathione redox cycle. 767 3


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