PubMed · 4924762
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K Nagano. 1970. [Transport function and cell membaane].. https://pubmed.ncbi.nlm.nih.gov/4924762/
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Although much has been learned about signal transduction mechanisms and binding proteins involved in lipopolysaccharides (LPS)-induced activation of monocytes/macrophages, little is known about the ability of internalized LPS to activate cells. To approach this question we either exposed macrophages to LPS or microinjected the cells with LPS before studying early cellular events associated with LPS-mediated macrophage activation. We measured membrane currents and translocation of NFkappaB to the nucleus. Using the whole-cell patch clamp technique ion channels were analyzed and characterized as K+ sensitive inward and outward currents. Exogenous LPS was shown to increase the voltage-dependent outward current whereas the voltage-dependent inward current was unaffected. However when cells were microinjected with LPS both inward and outward current were completely abolished. The presence of LPS within the cells did not prevent them to perform phagocytosis or to respond to fMLP with an appropriate increase in [Ca2+]i. The immunocytological detection of NFkappaB p65 translocation revealed that exogenous LPS led to the nuclear localization of the p65 subunit of NFkappaB, whereas only the cytoplasmic localization of p65 was observed following microinjection of LPS. These data show that one major process in macrophage activation, the NFkappaB dependent transcription of a number of genes encoding for many inflammatory mediators cannot be induced by intracellular LPS but requires the interaction of LPS with external membrane components. However intracellular LPS causes a drastic decrease in potassium currents which by keeping the cell membrane at a depolarized potential may result in changed biological answers of these cells.
In order to study the plant uptake and downward migration of radiostrontium and radiocesium deposited on to a flooded rice field, 85Sr and 137Cs were applied to the standing water over an acidic sandy soil in planted lysimeters. The plant uptake was quantified with the areal transfer factor (TFa, m2 kg(-1)-dry plant). Following the spiking 14 days after transplanting, the TFa values for the hulled seeds were 3.9 x 10(-4) for 85Sr and 1.4 x 10(-4) for 137Cs, whereas those for the straws were 1.3 x 10(-2) and 3.2 x 10(-4), respectively. The 137Cs TFa from the spiking at the anthesis/milky-ripe stage was several times higher than that from the earlier spiking, whereas the difference was much less in the 85Sr TFa. Such an increase in the 137Cs TFa was attributed mainly to an enhanced plant-base uptake. The addition of KCl and lime after the spiking significantly reduced the TFa values of both radionuclides. The reducing effect was greater for the later spiking. An appreciable fraction of the applied activity leached out of the lysimeter for 85Sr, whereas a negligible fraction leached for 137Cs. The leaching was remarkably increased by the KCl and lime addition for both. A conspicuous localization of 137Cs with respect to the soil surface was observed. In a batch experiment, the 137Cs concentration in the standing water decreased more rapidly than that of 85Sr, both of which were fitted to the power functions of the elapsed time. To add KCl and lime slowed such decreases to lessen the distribution coefficients (Kd) of both 85Sr and 137Cs.
Glucose transport activity and its possible regulation by reactive oxygen species in two Glut1-expressing megakaryocytic cell lines, MO7e and B1647, differing in cytokine sensitivity were compared. Results show that: (1) In MO7e cells, glucose transport rate increased in response to thrombopoietin, granulocyte-macrophage colony-stimulating factor, or stem cell factor, due to a decreased Km. (2) A higher Vmax value was determined in B1647 cells, owing to the relative higher abundance of Glut1 on the plasmalemma; in these cells no change in glucose transport rate was observed on cytokine treatment. (3) The basal level of intracellular ROS was higher in B1647 than in M07e cells, where ROS production was enhanced upon cytokine exposure. (4) Basal or stimulated ROS production and Glut1 activity were significantly reduced by pretreating both cell lines with EUK-134, a superoxide dismutase and catalase mimetic. (5) In MO7e cells, EUK-134 brought back to control levels the Km values obtained on cytokine treatment, whereas in B1647 cells the antioxidant drastically reduced Vmax by decreasing the Glut1 content of the plasma membrane. Our data suggest that differences in acute regulation of glucose transport activity in the two cell lines may be related to differences in amplitude and spatial organization of ROS production.