Acidification and Toxicity of Metals to Aquatic Biota

1985 ◽  
Vol 42 (12) ◽  
pp. 2034-2049 ◽  
Author(s):  
P. G. C. Campbel ◽  
P. M. Stokes
Keyword(s):  
Metal Speciation ◽  
Biological Response ◽  
Metal Availability ◽  
Ph Effects ◽  
Type I ◽  
Aquatic Biota ◽  
Dominant Effect ◽  
Biological Surfaces ◽  
Freshwater Acidification ◽  
Organism Interactions

Acidification of freshwaters can in principle influence metal–organism interactions in at least two ways: the decrease in pH may affect metal speciation in solution, or it may affect biological sensitivity at the level of the cell surface. We considered the possible effects of environmental acidification (pH 7–4) on (1) metal speciation in solution, (2) metal adsorption at biological surfaces, and (3) metal uptake by and toxicity to aquatic biota. Attention was focused on some 10 metals of potential concern in the context of freshwater acidification (Ag, Al, Cd, Co, Cu, Hg, Mn, Ni, Pb, Zn). For the four metals (Al, Cu, Hg, Pb) predicted to manifest speciation changes in the range pH 7–4, confirmatory experimental data are available for two (Cu, Pb). In the six remaining cases predicted to show little sensitivity to pH changes in this range, supporting experimental evidence exists for four metals (Ag, Cd, Mn, Zn). A pH-dependent biological response is documented over a realistic range of H+ and metal concentrations for 6 of the 10 metals considered (Al, Cd, Cu, Zn, and to a lesser extent, Hg and Pb). These six metals fall into two groups: those for which a decrease in pH results in a decreased biological response (type I behavior: Cd, Cu, Zn) and those for which the dominant effect of acidification is to increase metal availability (type II behavior: Pb). Data for the remaining two metals (Al, Hg) clearly reveal pH effects, but the results are too few and too inconsistent to allow generalizations.

Speciation metal speciation of Metals metal , Effects on Aquatic Biota

2012 ◽  
pp. 10051-10061
Author(s):  
James C. McGeer ◽  
D. Scott Smith ◽  
Kevin V. Brix ◽  
William J. Adams
Keyword(s):  
Metal Speciation ◽  
Aquatic Biota

Notch Alters Sumoylation To Govern GFI1 Protein Stability and Support Its Transcriptional Repression Function

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3793-3793
Author(s):  
Jason Singer ◽  
Daniel Andrade ◽  
Diana Bareyan ◽  
David McClellan ◽  
Helena Lucente ◽  
...  
Keyword(s):  
Transcriptional Repression ◽  
Conflicts Of Interest ◽  
System Development ◽  
Biological Response ◽  
Transcriptional Regulator ◽  
Nervous System Development ◽  
Type I ◽  
Wild Type ◽  
Sumoylation Site ◽  
T Lymphopoiesis

Abstract The zinc-finger (ZF) transcriptional repressors, Growth factor independence (GFI)-1 and -1B are master regulators of lineage allocation in hematopoietic, aerodigestive tract and central nervous system development. GFI family members share near invariant SNAG and ZF domains at their N- and C-termini, respectively. Their SNAG domains recruit Lysine Specific Demethylase (LSD)-1, a dominant effector of transcriptional repression by GFI proteins, while ZFs 3-5 of both GFI1 and GFI1B recognize a common consensus element in target promoters. A non-homologous linker separates the SNAG and ZF domains. Despite near identical DNA binding and co-factor recruitment characteristics, GFI family proteins direct distinct hematopoietic outcomes. Granulopoiesis requires Gfi1, and Gfi1 mutations cause severe congenital neutropenia (SCN) type II. Gfi1 is also necessary for T-lymphopoiesis and maintenance of the malignant phenotype in lymphoid leukemias and lymphomas. In contrast, Gfi1b specifies erythroid and megakaryocytic fates and is often abundantly expressed in myeloid leukemias. These distinct outcomes cannot be explained by patterns of expression alone, as Gfi1 and Gfi1B transcripts partially overlap during hematopoiesis. These findings suggest a need to distinguish between GFI family proteins as they integrate developmental signals to coordinate alternate hematopoietic fates. How this occurs is not understood. We hypothesized that functional differences between GFI1 and GFI1B may arise from interactions and post-translational modifications occurring uniquely within their linker regions. We show the GFI1 linker contains a type-I SUMOylation consensus motif centered on K239 that is absolutely conserved among mammalian GFI1 proteins but absent from GFI1B. K239 is required for robust GFI1 SUMOylation, as arginine substitution (K239R) significantly impairs formation of high molecular weight, SUMO-conjugated GFI1 derivatives. Coincidentally, K239R substitution also significantly impairs LSD1 recruitment by the GFI1 SNAG domain. The SUMOylation site in the GFI1 linker is contained within the binding site for PIAS3, an E3 SUMO ligase. PIAS3 co-expression antagonizes transcriptional repression by GFI1, but not GFI1B. The GFI1-K239R derivative represses transcription comparable to wild type GFI1, but resists the inhibitory effects of PIAS3. Moreover, GFI1-K239R preferentially co-purifies with chromatin in fractionated cells, displaying a prolonged half-life relative to wild type GFI1. These data suggest that GFI1 SUMOylation occurs on chromatin, facilitates LSD1 recruitment and serves as a prelude to GFI1 degradation. We surmised that the Notch1 intracellular domain (N1-ICD), which requires GFI1 for both normal and malignant T-lymphopoiesis, might alter GFI1 SUMOylation to reinforce its functions as a transcriptional regulator. We show that N1-ICD interacts directly with the GFI1 linker via the same motif that binds PIAS3. N1-ICD and PIAS3 compete for GFI1 binding and display an oppositional relationship in GFI1-mediated transcriptional repression. N1-ICD reinforces GFI1 as a transcriptional repressor, blocks GFI1 conjugation by ubiquitin family proteins and prevents GFI1 degradation. Our findings suggest a post-transcriptional mechanism by which Notch signaling endorses GFI1 as a transcriptional regulator and intimate GFI1 binding partners like LSD1 as candidate biological response modifiers in Notch-driven malignancies. Disclosures: No relevant conflicts of interest to declare.

Magnetic Alignment of Type I Collagen as a Method for Altering Tensile Mechanical Properties

2012 ◽  
Author(s):  
Tyler Novak ◽  
Jamie Canter ◽  
Dafang Chen ◽  
Joel Hungate ◽  
Sherry Voytik-Harbin ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Type I Collagen ◽  
Structural Integrity ◽  
Biological Response ◽  
Type I ◽  
Noninvasive Methods ◽  
Tissue Constructs ◽  
Musculoskeletal Tissues ◽  
Common Technique ◽  
Scaffold Materials

To date, ligament and tendon replacements largely utilize autograft/allograft transplantation, although the use of tissue engineered materials remain a promising solution [10]. The development of an engineered solution may depend on the choice of scaffold materials with optimal fiber alignment. Type I collagen is an abundant extracellular matrix component in musculoskeletal tissues. The controlled alignment of type I collagen for tissue engineering and regenerative medicine applications enables the fabrication of unique scaffolds that emulate the ultrastructure of their native counterparts. Moreover, the alignment of type I collagen has become a common technique to manipulate mechanical properties of tissue constructs and the biological response of embedded cells [1,2]. It is additionally important to develop noninvasive methods to align collagen structures while maintaining inherent structural integrity and biological activity.

scholarly journals A Conserved IFN-α Receptor Tyrosine Motif Directs the Biological Response to Type I IFNs

2008 ◽  
Vol 180 (8) ◽  
pp. 5483-5489 ◽  
Author(s):  
Wenli Zhao ◽  
Carolyn Lee ◽  
Rebecca Piganis ◽  
Courtney Plumlee ◽  
Nicole de Weerd ◽  
...  
Keyword(s):  
Biological Response ◽  
Type I ◽  
Type I Ifns

Voltammetric characterisation of macroalgae-exuded organic ligands (L) in response to Cu and Zn: a source and stimuli for L

2014 ◽  
Vol 11 (2) ◽  
pp. 100 ◽  
Author(s):  
Hollydawn Murray ◽  
Guillaume Meunier ◽  
Constant M. G. van den Berg ◽  
Rachel R. Cave ◽  
Dagmar B. Stengel
Keyword(s):  
Water Chemistry ◽  
Metal Speciation ◽  
Organic Ligands ◽  
Metal Availability ◽  
Conditional Stability ◽  
Laminaria Hyperborea ◽  
Metal Concentrations ◽  
Environmental Controls ◽  
Low Levels ◽  
Cu And Zn

Environmental context Identifying the source and stimuli responsible for organic ligands in seawater is crucial to understanding trace metal availability. Voltammetric techniques were employed to characterise the water chemistry of seaweed cultures exposed to low levels of Cu or Zn over 7 days. The results suggest that seaweeds are a potential source of metal complexing ligands and Cu and Zn appear to stimulate ligand production; further research is required to determine if this is applicable to macroalgae and metals outside this study. Abstract It is widely accepted that organic ligands control metal speciation in seawater, although little is known about their source, stimuli or identity. To gain insight on the possible environmental controls of metal complexing ligands (L), three brown macroalgae common in Irish waters (Ascophyllum nodosum, Fucus vesiculosus and Laminaria hyperborea) were cultured under low levels of Cu (0, 7.86 or 15.7nM) or Zn (0, 15.2 or 91.7nM) exposure. Seaweed chlorophyll-a fluorescence (Fv/Fm), metal speciation (Cu, Zn), complexing ligands (LM), conditional stability constants (logK′LM), glutathione (GSH), cysteine (Cys) and seaweed metal contents were monitored over 7 days. Although there was no effect on the internal seaweed metal concentrations, Cu and Zn additions significantly altered the water chemistry of each culture. Metal additions increased the total dissolved metal concentrations for all three species. Significantly higher [LM] values in cultures with added metals than the relevant controls point to both metals as stimuli of L production. All species released ligands in response to Cu or Zn exposure, indicating each seaweed is a relevant source of L. Comparison of logK′ values to those of previously determined ligands provides little evidence that the ligands reported here belong to the compounds identified as L in the literature.

scholarly journals Biological Response to Macroporous Chitosan-Agarose Bone Scaffolds Comprising Mg- and Zn-Doped Nano-Hydroxyapatite

2019 ◽  
Vol 20 (15) ◽  
pp. 3835 ◽  
Author(s):  
Paulina Kazimierczak ◽  
Joanna Kolmas ◽  
Agata Przekora
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Type I Collagen ◽  
Positive Impact ◽  
Biological Response ◽  
Type I ◽  
Matrix Mineralization ◽  
Zn Ions ◽  
Resultant Material

Modification of implantable scaffolds with magnesium and zinc for improvement of bone regeneration is a growing trend in the engineering of biomaterials. The aim of this study was to synthesize nano-hydroxyapatite substituted with magnesium (Mg2+) (HA-Mg) and zinc (Zn2+) (HA-Zn) ions in order to fabricate chitosan-agarose-hydroxyapatite (HA) scaffolds (chit/aga/HA) with improved biocompatibility. Fabricated biomaterials containing Mg2+ or Zn2+ were tested using osteoblasts and mesenchymal stem cells to determine the effect of incorporated metal ions on cell adhesion, spreading, proliferation, and osteogenic differentiation. The study was conducted in direct contact with the scaffolds (cells were seeded onto the biomaterials) and using fluid extracts of the materials. It demonstrated that incorporation of Mg2+ ions into chit/aga/HA structure increased spreading of the osteoblasts, promoted cell proliferation on the scaffold surface, and enhanced osteocalcin production by mesenchymal stem cells. Although biomaterial containing Zn2+ did not improve cell proliferation, it did enhance type I collagen production by mesenchymal stem cells and extracellular matrix mineralization as compared to cells cultured in a polystyrene well. Nevertheless, scaffolds made of pure HA gave better results than material with Zn2+. Results of the experiments clearly showed that modification of the chit/aga/HA scaffold with Zn2+ did not have any positive impact on cell behavior, whereas, incorporation of Mg2+ ions into its structure may significantly improve biocompatibility of the resultant material, increasing its potential in biomedical applications.

scholarly journals TGF-β1 Increases GDNF Production by Upregulating the Expression of GDNF and Furin in Human Granulosa-Lutein Cells

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 185 ◽  
Author(s):  
Jingwen Yin ◽  
Hsun-Ming Chang ◽  
Yuyin Yi ◽  
Yuanqing Yao ◽  
Peter C.K. Leung
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Kinase Inhibitors ◽  
Transforming Growth Factor ◽  
Biological Response ◽  
Follicular Development ◽  
Transforming Growth Factor Β1 ◽  
Type I ◽  
High Level ◽  
Tgf Β1

Glial cell line-derived neurotrophic factor (GDNF) is expressed at a high level in the human ovary and GDNF signaling is involved in the direct control of follicular activation and oocyte maturation. Transforming growth factor-β1 (TGF-β1) plays an important role in the regulation of various ovarian functions. Furin is an intracellular serine endopeptidase of the subtilisin family that is closely associated with the activation of multiple protein precursors. Despite the important roles of GDNF and TGF-β1 in the regulation of follicular development, whether TGF-β is able to regulate the expression and production of GDNF in human granulosa cells remains to be determined. The aim of this study was to investigate the effect of TGF-β1 on the production of GDNF and its underlying mechanisms in human granulosa-lutein (hGL) cells. We used two types of hGL cells (primary hGL cells and an established immortalized hGL cell line, SVOG cells) as study models. Our results show that TGF-β1 significantly induced the expression of GDNF and furin, which, in turn, increased the production of mature GDNF. Using a dual inhibition approach combining RNA interference and kinase inhibitors against cell signaling components, we showed that the TβRII type II receptor and ALK5 type I receptor are the principal receptors that mediated TGF-β1-induced cellular activity in hGL cells. Additionally, Sma- and Mad-related protein (SMAD)3 and SMAD4 are the downstream signaling transducers that mediate the biological response induced by TGF-β1. Furthermore, furin is the main proprotein convertase that induces the production of GDNF. These findings provide additional regulatory mechanisms by which an intrafollicular factor influences the production of another growth factor through a paracrine or autocrine interaction in hGL cells.

scholarly journals The tyrosine kinase receptors Ron and Sea control "scattering" and morphogenesis of liver progenitor cells in vitro.

1996 ◽  
Vol 7 (4) ◽  
pp. 495-504 ◽  
Author(s):  
E Medico ◽  
A M Mongiovi ◽  
J Huff ◽  
M A Jelinek ◽  
A Follenzi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tyrosine Kinase ◽  
Progenitor Cells ◽  
Type I Collagen ◽  
Growth Factor Receptor ◽  
Biological Response ◽  
Tyrosine Kinase Receptors ◽  
Type I ◽  
Macrophage Stimulating Protein

The mammalian RON and the avian sea genes encode tyrosine kinase receptors of poorly characterized biological functions. We recently identified macrophage-stimulating protein as the ligand for Ron; no ligand has yet been found for Sea. In this work we investigated the biological response to macrophage-stimulating protein in mouse liver progenitor cells expressing Ron. These cells were also transfected with a chimeric cDNA encoding the cytoplasmic domain of Sea, fused to the extracellular domain of Trk (nerve growth factor receptor). In the presence of nanomolar concentrations of the respective ligands, both receptors induced cell "scattering", extracellular matrix invasion, and DNA synthesis. When liver progenitor cells were grown in a tri-dimensional type-I collagen matrix, ligand-induced stimulation of either Ron or Sea induced sprouting of branched cell cords, evolving into ductular-like tubules. The motogenic, mitogenic, and morphogenic responses were also elicited by triggering the structurally related hepatocyte growth factor receptor (Met) but not epidermal growth factor or platelet-derived growth factor receptors. These data show that Ron, Sea, and Met belong to a receptor subfamily that elicits a distinctive biological response in epithelial cells.

Development of a Self-Oscillating Mechanical Model to Investigate the Biological Response of Human Vocal Fold Fibroblasts to Phono-Mimetic Stimulation

2014 ◽  
Author(s):  
Neda Latifi ◽  
Hossein K. Heris ◽  
Siavash Kazemirad ◽  
Luc Mongeau
Keyword(s):  
Mechanical Model ◽  
Vocal Fold ◽  
Biological Response ◽  
Vocal Folds ◽  
Collagen Type I ◽  
Positive Control ◽  
Type I ◽  
Cellular Functions ◽  
Cell Scaffold ◽  
Biomechanical Stimulation

The human vocal folds are subjected to complex dynamic biomechanical stimulation during phonation. The aim of the present study was to develop and evaluate an airflow-induced self-oscillating mechanical model, i.e., a bioreactor, which mimics the geometry and the mechanical microenvironment of the human vocal folds. The bioreactor consisted of two composite synthetic vocal fold replicas loaded into a custom-built airflow supplied tube. A cell-scaffold mixture was injected into cavities within the replicas. The folds were phonated using a variable speed centrifugal blower for two hours a day over a period of seven days. The static and dynamic subglottal pressures and the dynamic supraglottal pressure were monitored. A similar bioreactor without mechanical excitation was used as positive control. The cell-scaffold mixture was harvested for cell viability and collagen type I immunohistochemistry tests seven days after injection. The flow-induced self-oscillations of the vocal fold replicas were shown to produce mechanical excitations that are typical of those in the human vocal fold lamina propria during phonation. The results confirmed that human vocal fold fibroblasts survived inside the present bioreactor, and maintained cellular functions of protein production.

Sign in / Sign up

Export Citation Format

Share Document