A thermodynamic study of Cu++−Zn++ ion exchange in theNitella flexilis cell wall

Summary Exchange isotherms of Cu²⁺ vs Zn²⁺-ions were performed on the cell wall of a fresh water alga,Nitella flexilis. The relevant thermodynamic parameters are calculated. The cell wall absorbs copper selectively. The selectivity is explained by a stronger chelation of the cupric ion, due to the Jahn-Teller effect. The wall acts like a two-site model, based on the nature of the ligands: a first group of aminesites reacts exothermically and a second of hydroxylic-carboxylic sites of lower affinity, reacts endothermically.     

Effect of lectins on the interactions between human peripheral blood lymphocytes and monocytes

Interactions between normal human peripheral blood T lymphocytes and monocytes were investigated by measuring the in vitro cellular adherence of these cells in the presence and in the absence of mitogens. Concanavalin A (Con A), lentil lectin (Lc), and phytohemagglutinin (PHA) in mitogenic doses increased 15 to 20 times the binding of T lymphocytes to monocytes. The lectin-induced binding was similar to that produced by neuraminidase-gal-actose-oxidase treatment. A good correlation was found between the early cellular adherence induced by these lectins and by neuraminidase-galactose-oxidase and the blastogenesis of the T lymphocytes measured after 3 days of culture by [³H]thymidine uptake. However, wheat germ agglutinin (WGA), a nonmitogenic lectin, also increased the binding of T lymphocytes to monocytes. Addition of specific carbohydrates completely inhibited the cellular interactions induced by lectins. Peanut agglutinin (PNA) induced adherence of lymphocytes only after treatment of these cells with neuraminidase. Striking differences were not found between the lectin-induced adherence observed with autologous and heterologous cells. Killing of monocytes abolished entirely the lectin-induced adherence of lymphocytes, however killed T lymphocytes were still able to interact weakly with live monocytes. Dexamethasone was found to be a potent inhibitor of mitogen-induced cellular interactions.     

Na movements and their oscillations during fertilization and the cell cycle in sea urchin eggs

We have analysed in detail the Na⁺ content and Na⁺ influx during fertilization and first divisions of the sea urchin egg (Paracentrotus lividus) using a filtration technique devised to eliminate rapidly contamination by the Na⁺ of external sea water. In the first 5 min following fertilization the egg fills up with Na⁺ (+ 30%). Thereafter Na⁺ is extruded and the Na⁺ content stabilizes at about 60% of the unfertilized egg level by the second cleavage (2 h). The initial increase in Na⁺ content is due to a large increase in Na⁺ influx already detected at 20 sec. The Na⁺ influx reaches its maximum at 1 min and its minimum at 5 min. H⁺ excretion follows the same kinetics. A second increase in Na⁺ influx is noted 5–10 min after fertilization; it reaches its maximum at prophase metaphase (30 min) and its minimum during cleavage (60 min). These oscillations in Na⁺ influx were observed for the first three divisions. Fertilization also immediately stimulates the Na⁺ efflux which remains elevated throughout the cell cycle and is responsible for the depletion of the Na⁺ content of the embryos. Activation of the eggs by weak amine bases (5 mM NH₄Cl) which bypasses the early cortical reaction produces only a depletion in the Na⁺ content of the egg similar to that produced by fertilization. NH₄Cl also increases the Na⁺ influx soon after fertilization, although no transient variations are noted.     

Dérivés Monotritylés du D-xylose

Monotritylation of O-acetyl derivatives of D-xylopyranose and D-xylofuranose with trityl chloride in acetonitrile-pyridine gave the tri-O-acetyl derivatives of 1-,2-, 3-, and 5-O-trityl-D-xylofuranose and of 1-, 2-, 3-, and 4-O-trityl-D-xylopyranose which were required for the identification of the various monotrityl derivatives obtained in the tritylation at 50° of D-xylose with trityl chloride in pyridine or hexamethylphosphoric triamide-silver acetate.     

Control of the Ca2+-triggered bioluminescence of Veretillum cynomorium lumisomes

Calcium ions can trigger an emission of light from Veretillum cynomorium lumisomes (bioluminescent vesicles) under conditions where they are not lysed. This process does not require a metabolically-linked source of energy, but is dependent upon the nature of the ions present inside and outside the vesicles. The Ca²⁺-triggered bioluminescence is stimulated by an asymmetrical distribution of cations or anions. Either high internal sodium or high external chloride is required for the maximal effect. When sodium is present outside the structure and potassium inside, the slow inward diffusion of calcium is decreased. Unbalanced diffusion of internal cations also stimulates the bioluminescence, suggesting control of the calcium influx by an electrochemical gradient. It is assumed that rapid outward diffusion of sodium or inward diffusion of chloride generates an electrical potential difference (inside negative) which drives the Ca²⁺-influx. With purified lumisomes it has been shown that Ca²⁺-triggered bioluminescence and calcium uptake (presumably net uptake) were correlated. In two instances uptake of the lipophilic cation dibenzyldimethylammonium has given direct evidence for the existence of a potential difference. With NaCl-loaded vesicles, it has not been possible to demonstrate an uptake of lipophilic cations but experiments with ²²Na and ⁴²K indicated a higher rate of sodium efflux, in accord with the proposed hypothesis.     

Studies on the electrogenic action of acetylcholine with Torpedo marmorata electric organ: V. Qualitative correlation between pharmacological effects and equilibration processes of the cholinergic receptor protein as revealed by the structural probe quinacrine

When the differential fluorescence emission at 515 nm of receptor-rich membrane fragments from Torpedo marmorata labelled with quinacrine is followed by energy transfer, addition of a high concentration of an agonist such as 0.4 mm-carbamylcholine or 0.4 mm-phenyltrimethylammonium causes a fast (unresolved) increase of fluorescence intensity followed by a slow (minute range) decrease, which leads to a final stable level. On the other hand, a stepwise addition of agonist at low concentrations gives only a slow fluorescence increase. Antagonists, such as flaxedil and d-tubocurarine, at all the concentrations tested, bring about exclusively slow fluorescence increases. Decamethonium at 0.4 mm gives no slow reaction but only a fast (unresolved) increase without transient overshoot.Addition of a local anaesthetic reduces the amplitude of the fluorescence response to carbamylcholine. The α-toxin from Naja nigricollis does not cause any change of fluorescence intensity but blocks the effect of the cholinergic agonists and antagonists.Dissolution of the membrane fragments by a non-ionic detergent abolishes the fast transient reaction triggered by the agonists but preserves the slow ones observed in the presence of agonists or antagonists. The data are interpreted in terms of a three-state model, a revised version of the model of Katz & Thesleff (1957): the fast transient reaction brought about by the agonists being assigned to the “activation” of the receptor-ionophore complex and the slow one to its “desensitization”.