On Inhibiting Effect of Acetates and Acetic Acid on Living Cells of Nitella.

1927 ◽  
Vol 24 (9) ◽  
pp. 935-936 ◽  
Author(s):  
M. Irwin
Keyword(s):  
Acetic Acid ◽  
Living Cells ◽  
Inhibiting Effect

Nitrification: an old process, a new concern

1971 ◽  
Vol 24 ◽  
Author(s):  
W. H. Verstraete
Keyword(s):  
Culture Medium ◽  
Nitrogen Sources ◽  
Living Cells ◽  
Factors Affecting ◽  
Inhibiting Effect ◽  
Proteose Peptone ◽  
Asparaginase Activity

Some  factors affecting the L-asparaginase activity of E.  aroideae were investigated. Increasing  concentrations of glucose in the culture medium had an inhibiting effect on  the production of L-asparaginase by this microorganism. Buffering of the  culture medium in order to stabilize the pH during growth resulted in a decrease  of the L-asparaginase activity. From the different nitrogen sources examined,  tryptone, proteose peptone nr 2 and nr 3 stimulated the L-asparaginase  production. Toluene treatment of the cells practically destroyed the  L-asparaginase. Acetone dried cells showed an L-asparaginase activity  comparable with the activity of living cells.

scholarly journals Fibronectin binding to thrombin-stimulated platelets: evidence for fibrin(ogen) independent and dependent pathways

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 26-32
Author(s):  
EF Plow ◽  
GA Marguerie ◽  
MH Ginsberg
Keyword(s):  
Molecular Weight ◽  
Acetic Acid ◽  
Living Cells ◽  
Plasma Fibronectin ◽  
Divalent Ions ◽  
Fibrinogen Binding ◽  
Calcium Requirement ◽  
Variable Extent ◽  
Fibronectin Binding ◽  
Dependent Pathway

Plasma fibronectin binds in a specific and saturable manner to thrombin- stimulated platelets. gamma-Thrombin stimulated 80% as much fibronectin binding to platelets as alpha-thrombin with conversion of less than or equal to 1% of platelet fibrinogen to fibrin. Afibrinogenemic and normal platelets bound similar quantities of fibronectin in the presence of calcium or magnesium-ethylene glycol tetra-acetic acid (EGTA). These observations indicate that fibronectin can interact with platelets without involvement of fibrin or fibrinogen. Nevertheless, two different effects of fibrin(ogen) on fibronectin binding were observed. First, exogenous fibrinogen inhibited fibronectin binding to thrombin-stimulated platelets. This inhibition was unidirectional, as fibronectin did not inhibit fibrinogen binding to ADP or thrombin- stimulated cells. Second, formaldehyde-fixed cells with surface- associated fibrin bound significant quantities of fibronectin. This interaction required calcium and did not occur on fixed cells with or without surface-bound fibrinogen. A portion of the ligand bound to fixed cells with surface-associated fibrin was modified to form a derivative with a molecular weight identical to that of the fibronectin subunit cross-linked to the alpha-chain of fibrin. This high mol wt derivative was also observed to a variable extent with living cells in the presence of magnesium or calcium but not in the presence of magnesium-EGTA. Thus, fibronectin binds to platelets by at least two mechanisms: (1) a fibrin(ogen)-independent pathway that requires divalent ions and is inhibited by exogenous fibrinogen; and (2) a fibrin-dependent pathway with an absolute calcium requirement. With nonaggregated, thrombin-stimulated platelets, the former pathway appears to predominate.

Release of cotyledonary shoots of pea (Pisum sativum) seedlings from inhibition as related to endogenous zeatin and ethylene and exogenous IAA and benzyladenine

Biologia ◽  
2007 ◽  
Vol 62 (1) ◽  
Author(s):  
Helena Fišerová ◽  
Jiří Šebánek ◽  
Jan Hradilík ◽  
Petr Doležel ◽  
Zuzana Mikušová ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Pisum Sativum ◽  
Apical Dominance ◽  
The Other ◽  
Main Stem ◽  
Inhibiting Effect ◽  
Pea Seedlings ◽  
Exogenous Iaa

AbstractThis paper deals with apical dominance using a dicotylar model obtained after decapitation of pea seedlings with two shoots — one dominant and the other inhibited. When the dominant shoot was decapitated the inhibited one is released from inhibition and after 24 to 72 h begins to grow. However, the levels of trans-zeatin and production of ethylene increase within 4 and 6 hours respectively after release from inhibition, and within an interval of 72 h the levels of both phytohormones begin gradually to decrease. This indicates that also in this model, the release from apical dominance is associated with an increase in the level of cytokinin zeatin and, thereafter, also with an increased production of ethylene. If indolyl-3-acetic acid (IAA) is applied on the decapitated main stem after decapitation of the dominant shoot, the growth of the initially inhibited one is very strongly retarded; if, however, IAA is applied on the decapitated dominant shoot, this inhibition is significantly weaker. This means that the inhibiting effect of IAA on the inhibited shoot originates to a greater degree from the main stem rather than from the dominant shoot. The effect of benzyladenine (BA) is transferred equally from the decapitated main stem and from the decapitated dominant shoot because the initially inhibited shoot begins to grow as well as also other shoots from serial cotyledonary buds.

The Effects of the Chelating Agent Ethylenediamine Tetra-acetic Acid on Cell Adhesion in the Slime Mould Dictyostelium discoideum

Development ◽  
1959 ◽  
Vol 7 (3) ◽  
pp. 335-343
Author(s):  
Robert L. Dehaan
Keyword(s):  
Acetic Acid ◽  
Plasma Membrane ◽  
Cell Adhesion ◽  
Cell Surface ◽  
Dictyostelium Discoideum ◽  
Chelating Agent ◽  
Living Cells ◽  
Slime Mould ◽  
Chemical Mechanisms ◽  
Mechanical Separation

Certain properties of living cells appear to depend primarily on changes at, or characteristics of, the cell surface or plasma membrane. Among these ‘surfacelinked’ phenomena are to be classed adhesion of cells to their neighbours or substratum, pseudopodial activity and plasma membrane stability, and, frequently, cell and tissue movements. (Others which might be mentioned, such as pinocytosis, trans-membrane movements of substances, and vacoule formation, will not be considered here.) Attempts to examine these properties in terms of chemical mechanisms have not been notably successful, owing in part to the fact that the experimental material has traditionally been the tissues or embryos of metazoan forms. Thus, investigators have worked with heterogeneous and often constantly changing populations of cells, from which individual cells could be obtained only by the use of more or less deleterious methods such as mechanical separation or treatment with disaggregating agents.

scholarly journals THE EFFECT OF ACETATE BUFFER MIXTURES, ACETIC ACID, AND SODIUM ACETATE, ON THE PROTOPLASM, AS INFLUENCING THE RATE OF PENETRATION OF CRESYL BLUE INTO THE VACUOLE OF NITELLA

1927 ◽  
Vol 11 (2) ◽  
pp. 111-121 ◽  
Author(s):  
Marian Irwin
Keyword(s):  
Acetic Acid ◽  
Phosphate Buffer ◽  
Sodium Acetate ◽  
Ph Value ◽  
Specific Effect ◽  
Acetate Buffer ◽  
Rate Of Penetration ◽  
Cresyl Blue ◽  
Inhibiting Effect ◽  
Buffer Mixture

When living cells of Nitella are exposed to a solution of sodium acetate and are then placed in a solution of brilliant cresyl blue made up with a borate buffer mixture at pH 7.85, a decrease in the rate of penetration of dye is found, without any change in the pH value of the sap. It is assumed that this inhibiting effect is caused by the action of sodium on the protoplasm. This effect is not manifest if the dye solution is made up with phosphate buffer mixture at pH 7.85. It is assumed that this is due to the presence of a greater concentration of base cations in the phosphate buffer mixture. In the case of cells previously exposed to solutions of acetic acid the rate of penetration of dye decreases with the lowering of the pH value of the sap. This inhibiting effect is assumed to be due chiefly to the action of acetic acid on the protoplasm, provided the pH value of the external acetic acid is not so low as to involve an inhibiting effect on the protoplasm by hydrogen ions as well. It is assumed that the acetic acid either has a specific effect on the protoplasm or enters as undissociated molecules and by subsequent dissociation lowers the pH value of the protoplasm. With acetate buffer mixture the inhibiting effect is due to the action of sodium and acetic acid on the protoplasm. The inhibiting effect of acetic acid and acetate buffer mixture is manifested whether the dye solution is made up with borate or phosphate buffer mixture at pH 7.85. It is assumed that acetic acid in the vacuole serves as a reservoir so that during the experiment the inhibiting effect still persists.

scholarly journals Fibronectin binding to thrombin-stimulated platelets: evidence for fibrin(ogen) independent and dependent pathways

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 26-32 ◽  
Author(s):  
EF Plow ◽  
GA Marguerie ◽  
MH Ginsberg
Keyword(s):  
Molecular Weight ◽  
Acetic Acid ◽  
Living Cells ◽  
Plasma Fibronectin ◽  
Divalent Ions ◽  
Fibrinogen Binding ◽  
Calcium Requirement ◽  
Variable Extent ◽  
Fibronectin Binding ◽  
Dependent Pathway

Abstract Plasma fibronectin binds in a specific and saturable manner to thrombin- stimulated platelets. gamma-Thrombin stimulated 80% as much fibronectin binding to platelets as alpha-thrombin with conversion of less than or equal to 1% of platelet fibrinogen to fibrin. Afibrinogenemic and normal platelets bound similar quantities of fibronectin in the presence of calcium or magnesium-ethylene glycol tetra-acetic acid (EGTA). These observations indicate that fibronectin can interact with platelets without involvement of fibrin or fibrinogen. Nevertheless, two different effects of fibrin(ogen) on fibronectin binding were observed. First, exogenous fibrinogen inhibited fibronectin binding to thrombin-stimulated platelets. This inhibition was unidirectional, as fibronectin did not inhibit fibrinogen binding to ADP or thrombin- stimulated cells. Second, formaldehyde-fixed cells with surface- associated fibrin bound significant quantities of fibronectin. This interaction required calcium and did not occur on fixed cells with or without surface-bound fibrinogen. A portion of the ligand bound to fixed cells with surface-associated fibrin was modified to form a derivative with a molecular weight identical to that of the fibronectin subunit cross-linked to the alpha-chain of fibrin. This high mol wt derivative was also observed to a variable extent with living cells in the presence of magnesium or calcium but not in the presence of magnesium-EGTA. Thus, fibronectin binds to platelets by at least two mechanisms: (1) a fibrin(ogen)-independent pathway that requires divalent ions and is inhibited by exogenous fibrinogen; and (2) a fibrin-dependent pathway with an absolute calcium requirement. With nonaggregated, thrombin-stimulated platelets, the former pathway appears to predominate.

scholarly journals The production of auxin by dying cells

2021 ◽  
Author(s):  
A Rupert Sheldrake
Keyword(s):  
Cell Death ◽  
Organic Matter ◽  
Acetic Acid ◽  
Vascular Plants ◽  
Hydrolytic Enzymes ◽  
Living Cells ◽  
Tracheary Elements ◽  
Auxin Production ◽  
Dying Cells ◽  
Indole 3 Acetic Acid

Abstract In this review, I discuss the possibility that dying cells produce much of the auxin in vascular plants. The natural auxin, indole-3-acetic acid (IAA), is derived from tryptophan by a two-step pathway via indole pyruvic acid. The first enzymes in the pathway, tryptophan aminotransferases, have a low affinity for tryptophan and break it down only when tryptophan levels rise far above normal intracellular concentrations. Such increases occur when tryptophan is released from proteins by hydrolytic enzymes as cells autolyse and die. Many sites of auxin production are in and around dying cells: in differentiating tracheary elements; in root cap cells; in nutritive tissues that break down in developing flowers and seeds; in senescent leaves; and in wounds. Living cells also produce auxin, such as those transformed genetically by the crown gall pathogen. IAA may first have served as an exogenous indicator of the presence of nutrient-rich decomposing organic matter, stimulating the production of rhizoids in bryophytes. As cell death was internalized in bryophytes and in vascular plants, IAA may have taken on a new role as an endogenous hormone.

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