Copper and haemocyanin dynamics in aquatic invertebrates

1999 ◽  
Author(s):  
H. H. Taylor ◽  
Julie M. Anstiss
Keyword(s):  
Circulatory Arrest ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Copper Accumulation ◽  
Oxygen Binding ◽  
Midgut Gland ◽  
Branchial Heart ◽  
High Concentrations ◽  
And Function ◽  
Local Oxygen

Mechanisms of copper accumulation and detoxification, and of haemocyanin biosynthesis and catabolism, in aquatic arthropods and molluscs are reviewed. Crustacean haemocyanin transports copper in the blood by sequestering additional copper outside the oxygen-binding centre. Large changes in haemocyanin concentration in crustacean blood during moulting and hyposaline exposure generally reflect extracellular volume adjustments rather than biosynthesis and catabolism. Haemocyanin synthesis in decapod crustaceans is stimulated by hypoxia and, in an amphipod, by parasitization. Starvation causes breakdown of haemocyanin. Haemocyanin synthesis occurs principally in the midgut gland of crustaceans and in fixed blood cells (cyanocytes) that are located in certain tissues. It is hypothesized that cyanocytes provide a local oxygen reserve during circulatory arrest. Haemocyanin synthesis occurs primarily in the branchial glands of dibranchiate cephalopods but in the midgut gland of tetrabranchiates. Connective tissue pore cells are proposed as the site of haemocyanin synthesis in gastropods, although similar cells in cephalopod branchial hearts probably catabolize haemocyanin. Crustacean midgut glands contain copper-metallothioneins and glutathione, which donate Cu(I) to apohaemocyanin and function in detoxification and mineralization of excess copper. The physiological significance of high concentrations of quasi-crystalline haemocyanin within vascular spaces of the prosobranch left kidney, opisthobranch blood gland and cephalopod branchial heart appendage is discussed.

Abstract TP94: Mesenchymal Stromal Cells Behave Differently When Exposed to Medications Commonly Prescribed to Stroke Patients

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Nikunj Satani ◽  
Bing Yang ◽  
Duyen M Nghiem ◽  
Xiaopei Xi ◽  
Adrian P Gee ◽  
...  
Keyword(s):  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
High Glucose ◽  
Fold Increase ◽  
Stroke Recovery ◽  
Stroke Patients ◽  
Healthy Humans ◽  
Tnf Α ◽  
High Concentrations ◽  
And Function

Background: As a promising investigational therapy for stroke recovery, mesenchymal stromal cells (MSCs) are in various stages of clinical trials. MSCs may promote recovery through cytokine release and immunomodulation. Stroke patients typically are treated with antiplatelets and medications for hypertension and hyperlipidemia. We explored the effect of commonly prescribed drugs at physiological concentrations on MSCs. Methods: Clinical grade bone marrow MSCs from healthy donor at passage 2 were thawed and re-suspended in serum free media. Monocytes (Mo) were isolated from peripheral blood of healthy humans. MSCs and Mo were cultured alone as well as in co-culture and exposed to simvastatin, atenolol, losartan, captopril, or aspirin. They were also exposed to high glucose (upto 40mM) to simulate hyperglycemia. At 24 hours of incubation, media was collected and TNF-α concentration was measured, as an index of immunomodulation of Mo by MSCs. Cell viability was also measured (using MTT assay and flow cytometry). Results: There were significant effects of all drugs on viability of MSCs but with no impact on Mo. More importantly, Losartan (dose independent), Simvastatin and Atenolol (dose-dependent) reduced the viability of MSCs even at the pharmacologically relevant concentrations (Fig 1). High glucose had no effect on viability of MSCs or Mo. TNF-α secretion from co-culture of MSCs and Mo at 24 hours showed differences at very high doses of aspirin (2-fold increase), atenolol (0.5 fold decrease), and glucose (0.5 fold decrease) (data not shown). However, these high concentrations are unlikely to be achieved pharmacologically in plasma of patients treated with these drugs. Conclusion: Exposure of MSCs to clinically relevant drugs can alter their viability and function. Our results suggest that stroke trials involving use of intravenous MSCs should consider the differential impact of commonly prescribed medications on MSCs function.

Glycoprotein V-Deficient Platelets Have Undiminished Thrombin Responsiveness and Do Not Exhibit a Bernard-Soulier Phenotype

Blood ◽  
1999 ◽  
Vol 94 (12) ◽  
pp. 4112-4121 ◽  
Author(s):  
Mark L. Kahn ◽  
Thomas G. Diacovo ◽  
Dorothy F. Bainton ◽  
Francois Lanza ◽  
JoAnn Trejo ◽  
...  
Keyword(s):  
Wild Type ◽  
Spontaneous Bleeding ◽  
Atp Secretion ◽  
Platelet Receptor ◽  
High Concentrations ◽  
And Function ◽  
A1 Domain ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Adhesion Of Platelets

Abstract Adhesion of platelets to extracellular matrix via von Willebrand factor (vWF) and activation of platelets by thrombin are critical steps in hemostasis. Glycoprotein (GP) V is a component of the GPIb-V-IX complex, the platelet receptor for vWF. GPV is also cleaved by thrombin. Deficiency of GPIb or GPIX results in Bernard-Soulier syndrome (BSS), a bleeding disorder in which platelets are giant and have multiple functional defects. Whether GPV-deficiency might also cause BSS is unknown as are the roles of GPV in platelet-vWF interaction and thrombin signaling. We report that GPV-deficient mice developed normally, had no evidence of spontaneous bleeding, and had tail bleeding times that were not prolonged compared with wild-type mice. GPV-deficient platelets were normal in size and structure as assessed by flow cytometry and electron microscopy. GPV-deficient and wild-type platelets were indistinguishable in botrocetin-mediated platelet agglutination and in their ability to adhere to mouse vWF A1 domain. Platelet aggregation and ATP secretion in response to low and high concentrations of thrombin were not decreased in GPV-deficient platelets compared with wild-type. Our results show that (1) GPV is not necessary for GPIb expression and function in platelets and that GPV deficiency is not likely to be a cause of human BSS and (2) GPV is not necessary for robust thrombin signaling. Whether redundancy accounts for the lack of phenotype of GPV-deficiency or whether GPV serves subtle or as yet unprobed functions in platelets or other cells remains to be determined.

scholarly journals Regulation of murine copper homeostasis by members of the COMMD protein family

2020 ◽  
Vol 14 (1) ◽  
pp. dmm045963
Author(s):  
Amika Singla ◽  
Qing Chen ◽  
Kohei Suzuki ◽  
Jie Song ◽  
Alina Fedoseienko ◽  
...  
Keyword(s):  
Copper Homeostasis ◽  
Copper Accumulation ◽  
Copper Transporter ◽  
Copper Excretion ◽  
Copper Absorption ◽  
Hepatic Copper ◽  
High Copper ◽  
Molecular Machinery ◽  
And Function

ABSTRACTCopper is an essential transition metal for all eukaryotes. In mammals, intestinal copper absorption is mediated by the ATP7A copper transporter, whereas copper excretion occurs predominantly through the biliary route and is mediated by the paralog ATP7B. Both transporters have been shown to be recycled actively between the endosomal network and the plasma membrane by a molecular machinery known as the COMMD/CCDC22/CCDC93 or CCC complex. In fact, mutations in COMMD1 can lead to impaired biliary copper excretion and liver pathology in dogs and in mice with liver-specific Commd1 deficiency, recapitulating aspects of this phenotype. Nonetheless, the role of the CCC complex in intestinal copper absorption in vivo has not been studied, and the potential redundancy of various COMMD family members has not been tested. In this study, we examined copper homeostasis in enterocyte-specific and hepatocyte-specific COMMD gene-deficient mice. We found that, in contrast to effects in cell lines in culture, COMMD protein deficiency induced minimal changes in ATP7A in enterocytes and did not lead to altered copper levels under low- or high-copper diets, suggesting that regulation of ATP7A in enterocytes is not of physiological consequence. By contrast, deficiency of any of three COMMD genes (Commd1, Commd6 or Commd9) resulted in hepatic copper accumulation under high-copper diets. We found that each of these deficiencies caused destabilization of the entire CCC complex and suggest that this might explain their shared phenotype. Overall, we conclude that the CCC complex plays an important role in ATP7B endosomal recycling and function.

scholarly journals Cortical distal nephron Cl− transport in volume homeostasis and blood pressure regulation

2013 ◽  
Vol 305 (4) ◽  
pp. F427-F438 ◽  
Author(s):  
Susan M. Wall ◽  
Alan M. Weinstein
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Extracellular Volume ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Acid Base Balance ◽  
Relative Contribution ◽  
And Function

Renal intercalated cells mediate the secretion or absorption of Cl− and OH−/H+ equivalents in the connecting segment (CNT) and cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume, and blood pressure. Cl− absorption is either electrogenic and amiloride-sensitive or electroneutral and thiazide-sensitive. However, which Cl− transporter(s) are targeted by these diuretics is debated. While epithelial Na+ channel (ENaC) does not transport Cl−, it modulates Cl− transport probably by generating a lumen-negative voltage, which drives Cl− flux across tight junctions. In addition, recent evidence indicates that ENaC inhibition increases electrogenic Cl− secretion via a type A intercalated cells. During ENaC blockade, Cl− is taken up across the basolateral membrane through the Na+-K+−2Cl− cotransporter (NKCC1) and then secreted across the apical membrane through a conductive pathway (a Cl− channel or an electrogenic exchanger). The mechanism of this apical Cl− secretion is unresolved. In contrast, thiazide diuretics inhibit electroneutral Cl− absorption mediated by a Na+-dependent Cl−/HCO3− exchanger. The relative contribution of the thiazide and the amiloride-sensitive components of Cl− absorption varies between studies and probably depends on the treatment model employed. Cl− absorption increases markedly with angiotensin and aldosterone administration, largely by upregulating the Na+-independent Cl−/HCO3− exchanger pendrin. In the absence of pendrin [ Slc26a4 (−/−) or pendrin null mice], aldosterone-stimulated Cl− absorption is significantly reduced, which attenuates the pressor response to this steroid hormone. Pendrin also modulates aldosterone-induced changes in ENaC abundance and function through a kidney-specific mechanism that does not involve changes in the concentration of a circulating hormone. Instead, pendrin changes ENaC abundance and function, at least in part, by altering luminal HCO3−. This review summarizes mechanisms of Cl− transport in CNT and CCD and how these transporters contribute to the regulation of extracellular volume and blood pressure.

Effect of aortic clamping on proximal reabsorption and sodium excretion in the rat

1977 ◽  
Vol 232 (2) ◽  
pp. F92-F96 ◽  
Author(s):  
R. W. Osgood ◽  
N. H. Lameire ◽  
M. I. Sorkin ◽  
J. H. Stein
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Renal Perfusion ◽  
Ringer Solution ◽  
Aortic Clamping ◽  
Group I ◽  
Before And After

It has been suggested that aortic clamping prior to expansion of the extracellular fluid volume prevents the natriuretic response normally seen in this setting. To further evaluate this finding, two groups of re-collection micropuncture studies were performed before and after 7.5% body wt expansion with Ringer solution. Group I, immediate-clamp studies, n, 11. After control collections, perfusion pressure to the left kidney was decreased to 75 mmHg followed by Ringer loading. Group II, delayed-clamp studies, n, 8. After control collections, Ringer solution was given for 40 min. Then the left renal perfusion pressure was reduced to 75 mmHg and the Ringer infusion was continued at the same rate. In the immediate-clamp group, there was no change in total kidney glomerular filtration rate (GFR) (1.16 vs. 1.11 ml/min), nephron GFR (40 vs. 39 nl/min), tubular fluid-to-plasma inulin ratio (2.40 vs. 2.28), or filtrate delivery out of the proximal tubule (18 vs. 18 ndium excretion were not significantly altered. In the delayed-clamp studies, there was also no change in total or nephron GFR, but the tubular fluid-to-plasma inulin ratio fell from 2.52 to 1.65 (P less than .001) and distal delivery rose 9 nl/min after expansion (P less than .001). Sodium excretion increased 3.83 mueq/min and fractional sodium excretion rose 2.28%, both values being markedly greater than in the immediate-clamp studies (P less than .005 for both). These results demonstrate that immediate clamping obviates the fall in proximal reabsorption and the natriuretic response to Ringer loading and suggests that intrarenal adjustments are a major determinant of the magnitude of the natriuretic response to expansion of the extracellular volume

Structure and function in the excretory system of archaeogastropods and their significance in the evolution of gastropods

1985 ◽  
Vol 310 (1145) ◽  
pp. 383-406 ◽  
Keyword(s):  
Blood Supply ◽  
Renal Vein ◽  
Left Kidney ◽  
Structure And Function ◽  
Excretory System ◽  
Ultrastructural Organization ◽  
Primary Role ◽  
Partial Restoration ◽  
The Right ◽  
And Function

Three species of archaeogastropod mollusc, Monodonta lineata (da Costa), Emarginula reticulata Sowerby and Patella vulgata L. were selected as representative members of the Trochacea, Fissurellacea and Patellacea, respectively, for a comparative anatomical and ultrastructural study of the excretory system. Primary urine formation takes place by filtration of blood through the walls of the paired auricles in Monodonta and Emarginula and of the single auricle and ventricle in Patella . Urine then passes to right and left kidneys along the renopericardial canals. Contrary to earlier reports the two kidneys are different in structure and function in all three species, the larger right kidney retaining the primitive function of nitrogenous excretion, the left having a predominantly resorptive role and with a capacity to abstract from the blood solutes of larger molecular mass. The difference in the size of the two kidneys is exaggerated in Patella and Emarginula as a consequence of partial restoration of bilateral symmetry in these limpets. It has been possible to demonstrate at the ultrastructural level that the minute left kidney of Emarginula is functional. The vacuolated epithelial cells of the right kidney contain layered excretory spherules composed of purines, melanin and ferric iron in different proportions in the three genera. There is close similarity in the ultrastructural organization of these cells in Monodonta and Emarginula , but those of Patella show marked differences and their excretory spherules contain a higher proportion of melanin. The position of the left kidney in the mantle skirt, as exemplified by Monodonta , is believed to have arisen in the earliest gastropods correlated with the development of helical coiling. This was accompanied by a change in its blood vessels. It has lost its afferent renal vein, which primitively would have carried deoxygenated blood from the viscera, an arrangement which persists in the right kidney. The left efferent renal vein is reduced in Monodonta and lost in Patella and Emarginula . A new vessel has arisen linking left auricle and left kidney and there is evidence to suggest that it carries post-branchial oxygenated blood. It is believed to serve as both an afferent and major efferent route. The physiological implications of this change in the blood supply are discussed and held to be responsible for the functional differences between the two kidneys, creating conditions in the left which favour resorption of organic solutes and ions, and leaving the right kidney with the primary role of nitrogenous excretion. The evolution of the nephridial gland is examined in this context and is also believed to be correlated with the change in the blood supply to the left kidney. Ultrastructural evidence is given in support of its suggested resorptive function. The significance of the differences between right and left kidneys of archaeogastropods is discussed in relation to the evolution of the monotocardian excretory system, and the possible phylogenetic relationships of the groups of archaeogastropods are considered.

Peripheral Blood (PB) CD56bright and CD56dim Do Not Exhibit Differences in NKR Expression Compared to Their Cord Blood (CB) Counterparts: CB CD56dim May Represent an Intermediary between CB CD56bright and PB CD56dim.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 5155-5155
Author(s):  
Evan Shereck ◽  
Prakash Satwani ◽  
Carmella van de Ven ◽  
Janet Ayello ◽  
Ronald J. Wapner ◽  
...  
Keyword(s):  
Nk Cells ◽  
Magnetic Beads ◽  
Ex Vivo ◽  
Killer Cell ◽  
Receptor Expression ◽  
Becton Dickinson ◽  
Lectin Receptors ◽  
Cd16 Expression ◽  
High Concentrations ◽  
And Function

Abstract NK cells are characterized by absent CD3 and expression of CD56. CD56 NK cells are classified into CD56dim (90%) that are primarily cytotoxic, and CD56bright that secrete cytokines (Kaplan et al PNAS 1998; Shankaran et al Nature 2001). NK subsets carry out their respective functions based on their repertoire of NK receptors (NKRs), both activating and inhibiting (Moretta et al Annu Rev Immunol 2001). PB CD56dim cells express high concentrations of killer-cell immunoglobulin receptors (KIR) and C-type lectin receptors. PB CD56bright NK cells have increased expression of C-type lectin receptors, but have low expression of the KIRs (Nagler J. Immunol 1989). CD16 (the Fcγ receptor III or FcγRIII) which is responsible for binding to antibody-coated targets and initiating antibody-dependent cellular cytotoxicity (ADCC) has increased expression in CD56dim vs CD56bright NK cells (Leibson et al Immunity 1997). While the characterization and function of PB NK subsets and NKR expression are well described, there is little information regarding CB NK subsets and NKRs. We previously demonstrated a significant increase in CB NK NKR expression in ex-vivo engineered CB MNC following 48 hours of induction with IL-2, IL-7, IL-12, and Anti-CD3 (Ayello/Cairo et al BBMT 2006). In this study, we compared PB vs. CB NK subsets and NKR expression. PB and CB cells were positively selected for CD56+ using CD56 magnetic beads (Miltenyi, Aubrun, CA). CD56+ cells were sorted into CD3−/CD56bright and CD3−/CD56dim subsets by FACS sorter and NK receptor expression (CD16, CD158a {KIR2DL1} CD158a, h {KIR2DL1 and KIR2DS1}, CD158b {KIR2DL2}, CD161, NKG2A, NKG2C, NKG2D, Nkp44, NKp46, Becton Dickinson, Mountainview, CA,) of each subset was analyzed by flow cytometry. CD56+ selection yielded >89% purity (PB-96%, CB-89%). There was no statistical difference (mean ± SEM) in the receptor expression between the CB CD56bright and PB CD56bright and also between the CB CD56dim and PB CD56dim. However, PB CD56bright vs. PB CD56dim had increased expression of NKG2A (93.28 ± 2.83 vs. 66.64 ±7.74, p< 0.015), NKG2C (62.11 ±11.79 vs. 8.08 ± 2.98, p< 0.12), NKp44 (61.52 ±10.35 vs. 3.79 ± 2.32, p< 0.005) and NKp46 (92.53 ±3.31 vs. 64.66 ± 12.34, p< 0.05). PB CD56dim had increased expression of CD16 (93.30 ± 2.71 vs. 61.15 ± 11.79, p< 0.07) compared to PB CD56bright. The CB CD56dim compared to CB CD56bright has increased CD16 expression (85.06 ± 6.75 vs. 40.91 ± 5.74, p< 0.004) only. The PB CD56bright only differed from the CB CD56dim with respect to NKp44 (p< 0.021). The CB CD56bright differed from the PB CD56dim with respect to KIR2DL1 (p< 0.026), CD161 (p < 0.05), NKG2A (p < 0.025), and NKG2C (p < 0.05). In conclusion, there does appear to be a definite difference in NKR expression in PB CD56bright vs. PB CD56dim. However, PB vs. CB CD56dim and PB vs. CB CD56bright did not have any statistically significant NKR expression differences suggesting that the subsets have similar phenotypes in their respective cell source. Based on these results, we postulate that the CB CD56dim subset might reflect an intermediary step in development transitioning from CB CD56bright to PB CD56dim.

The Effects of Selenium on Toxicity of Copper on Rape

2012 ◽  
Vol 610-613 ◽  
pp. 288-291 ◽  
Author(s):  
Chun Yan Chao ◽  
Deng Jun Ma
Keyword(s):  
Metallic Copper ◽  
Experimental Treatment ◽  
Experimental Simulation ◽  
Copper Accumulation ◽  
Sewage Irrigation ◽  
Low Concentrations ◽  
The Law ◽  
High Concentrations ◽  
Soil Accumulation

To research the effect of how Se alleviate the harm brought by copper, we investigated the root length, stem, leaves, aberration by Cu colza in copper and Se-Cu compounds. The experimental simulation of sewage irrigation methods, the general consumption of rapeseed selected as experimental material, using the method of comparison, were dealing with a single copper, different concentrations selenium and copper concentrations were compared with experimental treatment. The Experiments were divided into three groups of treatment, respectively with a single copper, low concentrations selenium and copper and high concentrations of selenium and copper processing of rape. The focus is research the effect of selenium on the toxicity of copper. The result shows that the law of heavy metals like copper accumulation in the soil as well as in the migration and accumulation in rape and the law of metallic copper in the role of selenium in the soil accumulation as well as in the migration and accumulation in rape. The copper in the soil and rape are determinated by AAS. The results show that Selenium effectively alleviate the toxicity of copper on rape, and the ability of ease is high concentrations of selenium intensity than low concentrations of selenium.

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