scholarly journals A different sequence of events than previously reported leads to arsenic-induced damage in Ceratophyllum demersum L.

Metallomics ◽  
2014 ◽  
Vol 6 (3) ◽  
pp. 444-454 ◽  
Author(s):  
Seema Mishra ◽  
Hans-Joachim Stärk ◽  
Hendrik Küpper
Keyword(s):  
Time Course ◽  
Ceratophyllum Demersum ◽  
Ros Production ◽  
Sequence Of Events ◽  
Antenna Pigments ◽  
Photosynthetic Antenna ◽  
As Toxicity

Threshold and time course analysis of As toxicity revealed that damage to photosynthetic antenna pigments is most relevant at sublethal toxic As concentrations, while ROS production starts only at lethal concentrations.

PHYSIOLOGICAL RESPONSES OF THE CRAYFISH PACIFASTACUS LENIUSCULUS TO ENVIRONMENTAL HYPEROXIA: I. EXTRACELLULAR ACID-BASE AND ELECTROLYTE STATUS AND TRANSBRANCHIAL EXCHANGE

1989 ◽  
Vol 143 (1) ◽  
pp. 33-51 ◽  
Author(s):  
MICHÉLE G. WHEATLY
Keyword(s):  
Time Course ◽  
Extracellular Fluid ◽  
Respiratory Acidosis ◽  
Pacifastacus Leniusculus ◽  
Initial Increase ◽  
Flux Analysis ◽  
Freshwater Crayfish ◽  
Acid Base ◽  
Sequence Of Events ◽  
Fluid Compartment

Extracellular acid--base and ionic status, and transbranchial exchange of acidic equivalents and electrolytes, were monitored in freshwater crayfish (Pacifastacus leniusculus) during control normoxia (PO2 = 148 mmHg; 1 mmHg = 133.3 Pa), 72 h of hyperoxia (PO2 = 500 mmHg) and 24 h of recovery. An initial (3 h) respiratory acidosis of 0.2 pH units was completely compensated within 48 h by a 50% increase in metabolic [HCO3−+CO32-] accompanied by a significant reduction in circulating [Cl−]. In addition, the original increase in Pco2 was partially accommodated. The time course of transbranchial acidic equivalent exchange paralleled the change in extracellular metabolic base load with a significant branchial output of H+ during the first 48 h of hyperoxia. This was associated with net branchial effluxes of Cl− and Mg2+. Unidirectional flux analysis revealed parallel reductions in Na+ influx and efflux during initial hyperoxic exposure, reflecting an alteration in exchange diffusion. The net Cl− efflux was due to an initial increase in efflux followed by a reduction in influx. The reverse sequence of events occurred more rapidly when normoxia was reinstated: metabolic base was removed from the haemolymph and control haemolymph acid--base and ion levels were re-established within 24 h. Transbranchial fluxes of acidic equivalents similarly recovered within 24 h although net Na+ output and Cl− uptake persisted. The study attempted to identify relationships between branchial net H+ exchange and components of Na+ and Cl− exchange and quantitatively to correlate changes in the acidic equivalent and electrolyte concentrations in the extracellular fluid compartment with those in the external water.

Effect of a single air dive on pulmonary diffusing capacity in professional divers

1993 ◽  
Vol 74 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Z. Dujic ◽  
D. Eterovic ◽  
P. Denoble ◽  
G. Krstacic ◽  
J. Tocilj ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Time Course ◽  
Blood Gases ◽  
Diffusing Capacity ◽  
Pulmonary Diffusing Capacity ◽  
Sequence Of Events ◽  
Arterial Blood ◽  
Bubble Detection ◽  
Venous Gas Embolism ◽  
Arterial Po2

The aim of this study was to determine whether venous gas embolism after a single air dive, evaluated using precordial Doppler monitoring, was associated with alterations in spirometry, lung volumes, arterial blood gases, or pulmonary diffusing capacity for carbon monoxide (DLCO). Postdive time course monitoring of pulmonary function was undertaken in 10 professional divers exposed to absolute air pressure of 5.5 bar for 25 min in a dry walk-in chamber. The US Navy decompression table was followed. Venous bubbles were detected by precordial Doppler monitoring. Two types of decompression were used: air and 100% O2 applied for 21 min during decompression stops. Spirometry, flow-volume, and body plethysmography parameters were unchanged after the dive with air decompression (AD) as well as with O2 decompression (OD). A significant reduction in arterial PO2, on average 20 Torr, was found after the dive with AD. DLCO was decreased in all divers 20, 40, 60, and 80 min after diving with AD (P < 0.001), whereas it was not significantly decreased after diving with OD. Maximal DLCO decrease of approximately 15% occurred 20 min postdive. In AD diving, maximum bubble grade for each individual vs. maximum DLCO reduction correlated significantly (r = 0.85, P = 0.002), as well as DLCO vs. arterial PO2 (r = 0.64, P = 0.017). In conclusion, a reduction in pulmonary diffusing capacity is observed in parallel with the appearance of venous bubbles detected by precordial Doppler. We suggest that bubbles cause pulmonary microembolization, triggering a complex sequence of events that remains to be resolved. Measuring DLCO complements Doppler bubble detection in postdiving assessment of pulmonary function.

scholarly journals A study of novel lectins and their involvement in the activation of the prophenoloxidase system in Blaberus discoidalis

1995 ◽  
Vol 310 (1) ◽  
pp. 23-31 ◽  
Author(s):  
C Chen ◽  
H J Durrant ◽  
R P Newton ◽  
N A Ratcliffe
Keyword(s):  
Binding Sites ◽  
Serine Proteases ◽  
Time Course ◽  
Lectin Binding ◽  
Active Form ◽  
Reaction System ◽  
Activation Process ◽  
Blaberus Discoidalis ◽  
Sequence Of Events ◽  
Prophenoloxidase System

Endogenous and exogenous lectins have been found to activate the prophenoloxidase (proPO) system of the cockroach, Blaberus discoidalis, to the same extent as laminarin, a previously known microbial activator of proPO. The lectins can also further enhance this laminarin activation of the proPO system. Non-lectin proteins did not display any activation properties. The time course of proPO activation was studied after reconstitution of the reaction system using purified lectins, a trypsin-like enzyme, a trypsin inhibitor and partially purified lectin-binding proteins from the cockroach haemolymph. Lectin activation of the proPO system is probably not mediated by the lectin sugar-binding sites, as specific inhibitory sugars failed to abrogate the enhanced effect. The results suggest that alternative binding site(s) on the lectins may be involved in the proPO activation process. Evidence also suggests that several different lectins are involved in the regulation of the proPO system through separate receptors or binding molecules on the haemocytes, and that they exert their effects early in the sequence of events leading to conversion of proPO into its active form, possibly via regulation of serine proteases and protease inhibitors.

scholarly journals Osmotic and phorbol ester-induced activation of Na+/H+ exchange: possible role of protein phosphorylation in lymphocyte volume regulation.

1985 ◽  
Vol 101 (1) ◽  
pp. 269-276 ◽  
Author(s):  
S Grinstein ◽  
S Cohen ◽  
J D Goetz ◽  
A Rothstein
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Phorbol Ester ◽  
Time Course ◽  
Phorbol Esters ◽  
Underlying Mechanism ◽  
Atp Depletion ◽  
Sequence Of Events ◽  
Kinase C ◽  
Stimulation Of

The Na+/H+ antiport is stimulated by 12-O-tetradecanoylphorbol-13, acetate (TPA) and other phorbol esters in rat thymic lymphocytes. Mediation by protein kinase C is suggested by three findings: (a) 1-oleoyl-2-acetylglycerol also activated the antiport; (b) trifluoperazine, an inhibitor of protein kinase C, blocked the stimulation of Na+/H+ exchange; and (c) activation of countertransport was accompanied by increased phosphorylation of specific membrane proteins. The Na+/H+ antiport is also activated by osmotic cell shrinking. The time course, extent, and reversibility of the osmotically induced and phorbol ester-induced responses are similar. Moreover, the responses are not additive and they are equally susceptible to inhibition by trifluoperazine, N-ethylmaleimide, and ATP depletion. The extensive analogies between the TPA and osmotically induced effects suggested a common underlying mechanism, possibly activation of a protein kinase. It is conceivable that osmotic shrinkage initiates the following sequence of events: stimulation of protein kinase(s) followed by activation of the Na+/H+ antiport, resulting in cytoplasmic alkalinization. The Na+ taken up through the antiport, together with the HCO3- and Cl- accumulated in the cells as a result of the cytoplasmic alkalinization, would be followed by osmotically obliged water. This series of events could underlie the phenomenon of regulatory volume increase.

Mechanism of glucocorticoid-induced oxidative stress in rat hippocampal slice cultures

2009 ◽  
Vol 87 (6) ◽  
pp. 440-447 ◽  
Author(s):  
Jung-Man You ◽  
Su-Jin Yun ◽  
Kyong Nyon Nam ◽  
Chulhun Kang ◽  
Ran Won ◽  
...  
Keyword(s):  
Cell Death ◽  
Hippocampal Neurons ◽  
Time Course ◽  
Glucocorticoid Receptors ◽  
Hippocampal Slice ◽  
Pcr Analysis ◽  
Ros Generation ◽  
Hippocampal Damage ◽  
Ros Production ◽  
Hippocampal Slice Cultures

Prolonged stress results in elevation of glucocorticoid (GC) hormones, which can have deleterious effects in the brain. The hippocampus, which has a high concentration of glucocorticoid receptors, is especially vulnerable to increasing levels of GCs. GCs have been suggested to endanger hippocampal neurons by exacerbating the excitotoxic glutamate–calcium–reactive oxygen species (ROS) cascade. In an effort to reveal the mechanisms underlying GC-mediated hippocampal neurotoxicity, we aimed to clarify the molecular pathway of GC-induced ROS increase by using organotypic hippocampal slice cultures. Assays for ROS, using 2′,7′-dichlorodihydrofluorescein diacetate fluorescence, showed that treatment of synthetic GC, dexamethasone (DEX) significantly enhanced ROS levels. Time course and dose response analyses indicated that peak amount of ROS was generated at 4 h after treatment with 50 µmol/L DEX. By contrast, other steroid hormones, progesterone and estradiol did not influence ROS production. N-acetyl-l-cysteine completely suppressed ROS produced by DEX. Propidium iodide staining exhibited prominent cell death in the hippocampal layer after 96 h of DEX treatment. RU486, a GC receptor antagonist, almost completely blocked the effect of DEX on ROS production and cell death, indicating that DEX-induced ROS overproduction and hippocampal death are mediated via GC receptors. Real-time reverse transcriptase PCR analysis demonstrated that after DEX treatment the level of glutathione peroxidase mRNA was decreased whereas that of NADPH oxidase mRNA was significantly enhanced. These findings suggest that excess GCs cause hippocampal damage by regulating genes involved in ROS generation.

scholarly journals Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice in vivo

2012 ◽  
Vol 209 (4) ◽  
pp. 819-835 ◽  
Author(s):  
Marie-Luise von Brühl ◽  
Konstantin Stark ◽  
Alexander Steinhart ◽  
Sue Chandraratne ◽  
Ildiko Konrad ◽  
...  
Keyword(s):  
Time Course ◽  
Cardiovascular Death ◽  
Epifluorescence Microscopy ◽  
Factor Xii ◽  
Blood Monocytes ◽  
Extrinsic Pathway ◽  
Genetic Ablation ◽  
Vein Thrombosis ◽  
Sequence Of Events

Deep vein thrombosis (DVT) is a major cause of cardiovascular death. The sequence of events that promote DVT remains obscure, largely as a result of the lack of an appropriate rodent model. We describe a novel mouse model of DVT which reproduces a frequent trigger and resembles the time course, histological features, and clinical presentation of DVT in humans. We demonstrate by intravital two-photon and epifluorescence microscopy that blood monocytes and neutrophils crawling along and adhering to the venous endothelium provide the initiating stimulus for DVT development. Using conditional mutants and bone marrow chimeras, we show that intravascular activation of the extrinsic pathway of coagulation via tissue factor (TF) derived from myeloid leukocytes causes the extensive intraluminal fibrin formation characteristic of DVT. We demonstrate that thrombus-resident neutrophils are indispensable for subsequent DVT propagation by binding factor XII (FXII) and by supporting its activation through the release of neutrophil extracellular traps (NETs). Correspondingly, neutropenia, genetic ablation of FXII, or disintegration of NETs each confers protection against DVT amplification. Platelets associate with innate immune cells via glycoprotein Ibα and contribute to DVT progression by promoting leukocyte recruitment and stimulating neutrophil-dependent coagulation. Hence, we identified a cross talk between monocytes, neutrophils, and platelets responsible for the initiation and amplification of DVT and for inducing its unique clinical features.

Optical studies of biochemical events in the electric organ of Electrophorus

1964 ◽  
Vol 160 (979) ◽  
pp. 211-245 ◽  
Keyword(s):  
Time Course ◽  
Thermal Studies ◽  
Fluorescence Emission ◽  
Electric Organ ◽  
Emission Spectra ◽  
Creatine Phosphate ◽  
Fluorescence Response ◽  
Sequence Of Events ◽  
Oxidation Reduction

When slices of the main electric organ of Electrophorus are stimulated electrically, three different effects can be detected optically. These are: (1) A large decrease in absorption evidently due to a decrease of light scattering within the tissue; this change increases gradually with decreasing wavelength. (2) A decrease in absorption which has a definite peak at about 420 nm and is interpreted as arising from oxidation of a haemoprotein. (3) A diphasic (under some conditions triphasic) change in fluorescence emission, interpreted as arising from oxidation/reduction of diphosphopyridine nucleotide. This paper is mainly concerned with an examination of the third of these effects. Identification of the fluorescence response with reduction of DPN was supported by determination of excitation and emission spectra of resting tissue at room temperatures and at the temperature of liquid nitrogen. The emission spectrum of the fluorescence change after stimulation was also determined with a differential spectrofluorometer. The results of the fluorometry agreed well with those obtained by direct chemical analysis. The time course of the fluorescence response and the effect on it of various factors such as amount of stimulation, interval between periods of stimulation, direction of observation, electrical load, temperature, exclusion of oxygen and inhibitors of oxidative metabolism and glycolysis, are described in some detail. A combination of these observations with the results of chemical analyses and thermal studies supports the view that the sequence of events on stimulation of the electric organ is: (1) changes in internal ionic concentrations resulting from the flow of electric current: (2) activation of the sodium pump, driven by phosphate-bond energy and drawing initially on the reservoir provided by creatine phosphate; (3) activation of glycogenolysis to restore the ATP/ADP ratio. The bearing of the changes observed in the DPNH/DPN ratio on the mechanism by which glycogenolysis is controlled is discussed briefly.

scholarly journals Evaluation of oxidative status in acetaminophen treated rat hepatocytes in culture

2009 ◽  
pp. 239-246
Author(s):  
T Roušar ◽  
O Kučera ◽  
P Křiváková ◽  
H Lotková ◽  
R Kanďár ◽  
...  
Keyword(s):  
Functional Capacity ◽  
Time Course ◽  
Rat Hepatocytes ◽  
Oxidative Status ◽  
Ros Production ◽  
Cellular Viability ◽  
Time Intervals ◽  
Leakage Test ◽  
Cultured Rat Hepatocytes ◽  
In Cells

The present study describes the estimation of acetaminophen (AAP) toxicity in cultured rat hepatocytes. We used different concentrations of AAP – 1, 2.5, 5, 10 and 20 mM, to test influence of AAP on cellular viability, functional capacity and oxidative status at given time intervals. WST-1 test showed decrease of dehydrogenase activity in 5, 10 and 20 mM AAP to 75 % of control values after 1 hour of incubation. At 12 h of treatment, all AAP concentrations decreased WST-1 signal; no enzyme activity was found since 18 h in cells treated with 20 mM AAP according to LDH leakage test performed at 24 h of incubation. Functional capacity was tested by albumin assay where the decrease was strictly related to AAP dose. Intracellular oxidative status was assessed by analysis of GSH/GSSG levels and time course of ROS production and glutathione reductase (GR) activity. Increased ROS production was found already after 3 h of incubation in 2.5, 5, 10 and 20 mM AAP, respectively. The highest ROS production was measured after 12 h treatment. GR activity was decreased already after 3 h of incubation and remained also decreased in cells treated with 2.5, 5, 10 and 20 mM AAP during further incubation.

Mechanism of insulin-induced activation of Na(+)-K(+)-ATPase in isolated rat soleus muscle

1991 ◽  
Vol 261 (2) ◽  
pp. C224-C230 ◽  
Author(s):  
E. Weil ◽  
S. Sasson ◽  
Y. Gutman
Keyword(s):  
Soleus Muscle ◽  
Time Course ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Insulin Stimulation ◽  
K Uptake ◽  
Sequence Of Events ◽  
Rat Soleus Muscle ◽  
Isolated Rat ◽  
Stimulation Of

Insulin augments Na(+)-K(+)-ATPase activity in skeletal muscles. It has been proposed that the sequence of events is activation of Na(+)-H+ antiporter, increased intracellular Na+ concentration ( [Na+]i), and stimulation of Na(+)-K+ pump. We have used isolated rat soleus muscles to test this hypothesis. Insulin increased the ouabain-suppressible K+ uptake in a dose- and time-dependent manner. The maximal effect was observed at 50-100 mU/ml insulin. Stimulation of K+ uptake was accompanied by increased specific [3H]ouabain binding and lowered [Na+]i. The ionophore monensin, which promotes Na(+)-H+ exchange, also increased the rate of ouabain-suppressible K+ uptake in soleus muscle, with a maximal effect obtained at 10-100 microM ionophore. However, this increase was accompanied by an elevation of [Na+]i. In the presence of 10-100 microM monensin, addition of 100 mU/ml insulin further increased K+ uptake but reduced [Na+]i. The effect on K+ uptake was additive. Ouabain (10(-3) M) completely suppressed the effect of insulin on [Na+]i. Insulin had no effect on the magnitude or the time course of insulin stimulation of K+ uptake. Thus equal stimulation of Na(+)-K(+)-ATPase by insulin was observed when [Na+]i was elevated (under monensin) or lowered (under amiloride). These data suggest that activation of Na(+)-K(+)-ATPase in soleus muscle by insulin is not secondary to stimulation of Na(+)-H+ antiporter.

Role of lipid peroxidation in H2O2-induced renal epithelial (LLC-PK1) cell injury

1995 ◽  
Vol 268 (1) ◽  
pp. F30-F38 ◽  
Author(s):  
A. K. Salahudeen
Keyword(s):  
Lipid Peroxidation ◽  
Renal Cell ◽  
Time Course ◽  
Cell Injury ◽  
Thiobarbituric Acid ◽  
Alpha Tocopherol ◽  
In Vivo Studies ◽  
Sequence Of Events

The exact sequence of events or mechanisms by which H2O2 induces renal cell injury remains undetermined. Specifically, whether the attendant lipid peroxidation is a cause or an effect remains unclear. Employing H2O2 and LLC-PK1 cells, we tested the hypothesis that lipid peroxidation is a seminal event and that its inhibition is cytoprotective. In a time course study, lipid peroxidation (thiobarbituric acid reaction) and degradation (release of [3H]arachidonic acid) preceded H2O2-induced cytolysis (51Cr and lactate dehydrogenase release). The role of preceding lipid peroxidation in cytolysis was examined with lipid radical scavengers. alpha-Tocopherol and lazaroid compound 2-methyl aminochroman dose-dependently inhibited H2O2-induced lipid peroxidation and prevented cytolysis. 2-Methyl aminochroman cytoprotection was associated with blockade of lipid degradation. 21-Aminosteroid, another lazaroid, also inhibited lipid peroxidation and prevented cytolysis. These findings provide evidence that lipid alterations contribute to H2O2-mediated LLC-PK1 injury and, for the first time, demonstrate the potency of lazaroids in a renal cell line. In vivo studies with lazaroids may define the role of lipid peroxidation in acute renal injury models.

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