scholarly journals Effect of Sodium on Potassium Fluxes at the Cell Membrane and Vacuole Membrane of Red Beet

1971 ◽  
Vol 47 (6) ◽  
pp. 731-734 ◽  
Author(s):  
Ronald J. Poole
Nature ◽  
1990 ◽  
Vol 343 (6258) ◽  
pp. 567-570 ◽  
Author(s):  
J. Alexandra ◽  
J. P. Lassalles ◽  
R. T. Kado

1992 ◽  
Vol 102 (3) ◽  
pp. 527-532 ◽  
Author(s):  
A.R. Dluzewski ◽  
G.H. Mitchell ◽  
P.R. Fryer ◽  
S. Griffiths ◽  
R.J. Wilson ◽  
...  

We have attempted to determine whether the parasitophorous vacuole membrane, in which the malaria parasite (merozoite) encapsulates itself when it enters a red blood cell, is derived from the host cell plasma membrane, as the appearance of the invasion process in the electron microscope has been taken to suggest, or from lipid material stored in the merozoite. We have incorporated into the red cell membrane a haptenic phospholipid, phosphatidylethanolamine, containing an NBD (N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)) group, substituted in the acyl chain, and allowed it to translocate into the inner bilayer leaflet. After invasion of these labelled cells by the parasite, Plasmodium falciparum, immuno-gold electron microscopy was used to follow the distribution of the labelled lipid; this was found to be overwhelmingly in favour of the host cell membrane relative to the parasitophorous vacuole. Merozoites of P. knowlesi were allowed to attach irreversibly to red cells without invasion, using the method of pretreatment with cytochalasin. The region of contact between the merozoite and the host cell membrane was in all cases devoid of the labelled phosphatidylethanolamine. These results lead us to infer that the parasitophorous vacuole membrane is derived wholly or partly from lipid preexisting in the merozoite.


1972 ◽  
Vol 50 (6) ◽  
pp. 1415-1420 ◽  
Author(s):  
G. A. White ◽  
E. Taniguchi

The phytotoxin, helminthosporal (H-al), can damage the permeability of plant cell membranes and it is suggested that this may be an important factor in the susceptibility or predisposition of cereal tissues to attack by Bipolaris sorokiniana, the fungus which produces the toxin. Helminthosporal was tested for its effect on the apparent free space (AFS) of barley roots and the efflux of betacyanin from red beet root tissue. Cell membrane disruption was indicated by an increase in the AFS of H-al-treated barley roots. The effect of H-al on the AFS of barley roots did not appear to be correlated with respiratory inhibition by the toxin since cyanide, azide, and 2,4-dinitrophenol failed to increase the AFS. Oxygen uptake by red beet root tissue was strongly inhibited by H-al at concentrations of 1.0 mM and 2.0 mM, and was accompanied by an immediate and large efflux of betacyanin. No correlation was found, however, between the extent of respiratory inhibition and the amount of pigment released. Helminthosporal reacts directly with both the plasmalemma and the tonoplast membranes of the beet root cell, exclusive of effects on respiration, since the loss of betacyanin was equally rapid under aerobic or anaerobic conditions. The integrity of the beet cell tonoplast membrane appeared to be unrelated to respiration and energy supply. Calcium ions, which act to stabilize membranes, partially alleviated the loss of pigment from red beet tissue exposed to n-propanol and H-al. Permeability change in the plant cell membrane may be as important in the mode of action of H-al as are the effects of the toxin on respiration and oxidative phosphorylation.


Author(s):  
M. Ashraf ◽  
L. Landa ◽  
L. Nimmo ◽  
C. M. Bloor

Following coronary artery occlusion, the myocardial cells lose intracellular enzymes that appear in the serum 3 hrs later. By this time the cells in the ischemic zone have already undergone irreversible changes, and the cell membrane permeability is variably altered in the ischemic cells. At certain stages or intervals the cell membrane changes, allowing release of cytoplasmic enzymes. To correlate the changes in cell membrane permeability with the enzyme release, we used colloidal lanthanum (La+++) as a histological permeability marker in the isolated perfused hearts. The hearts removed from sprague-Dawley rats were perfused with standard Krebs-Henseleit medium gassed with 95% O2 + 5% CO2. The hypoxic medium contained mannitol instead of dextrose and was bubbled with 95% N2 + 5% CO2. The final osmolarity of the medium was 295 M osmol, pH 7. 4.


Author(s):  
J. J. Paulin

Movement in epimastigote and trypomastigote stages of trypanosomes is accomplished by planar sinusoidal beating of the anteriorly directed flagellum and associated undulating membrane. The flagellum emerges from a bottle-shaped depression, the flagellar pocket, opening on the lateral surface of the cell. The limiting cell membrane envelopes not only the body of the trypanosome but is continuous with and insheathes the flagellar axoneme forming the undulating membrane. In some species a paraxial rod parallels the axoneme from its point of emergence at the flagellar pocket and is an integral component of the undulating membrane. A portion of the flagellum may extend beyond the anterior apex of the cell as a free flagellum; the length is variable in different species of trypanosomes.


Author(s):  
A. C. Enders

The alteration in membrane relationships seen at implantation include 1) interaction between cytotrophoblast cells to form syncytial trophoblast and addition to the syncytium by subsequent fusion of cytotrophoblast cells, 2) formation of a wide variety of functional complex relationships by trophoblast with uterine epithelial cells in the process of invasion of the endometrium, and 3) in the case of the rabbit, fusion of some uterine epithelial cells with the trophoblast.Formation of syncytium is apparently a membrane fusion phenomenon in which rapid confluence of cytoplasm often results in isolation of residual membrane within masses of syncytial trophoblast. Often the last areas of membrane to disappear are those including a desmosome where the cell membranes are apparently held apart from fusion.


Author(s):  
M. W. Brightman

The cytological evidence for pinocytosis is the focal infolding of the cell membrane to form surface pits that eventually pinch off and move into the cytoplasm. This activity, which can be inhibited by oxidative and glycolytic poisons, is performed only by cell processes that are at least 300A wide. However, the interpretation of such toxic effects becomes equivocal if the membrane invaginations do not normally lead to the formation of migratory vesicles, as in some endothelia and in smooth muscle. The present study is an attempt to set forth some conditions under which pinocytosis, as distinct from the mere inclusion of material in surface invaginations, can take place.


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