scholarly journals DELAYED POTASSIUM EFFECT IN NITELLA

1938 ◽  
Vol 22 (1) ◽  
pp. 107-113 ◽  
Author(s):  
S. E. Hill ◽  
W. J. V. Osterhout

In normal cells of Nitella replacement of NaCl by KCl makes the P.D. much less positive: this is called the potassium effect. Cells which have lost the potassium effect usually show little or no change of P.D. when NaCl is replaced by KCl but an occasional cell responds after a delay. It seems possible that the delay may be largely due to the time required for potassium to combine with an organic substance, thus forming a compound which sensitizes the protoplasmic surface to the action of potassium.

1935 ◽  
Vol 18 (5) ◽  
pp. 687-694 ◽  
Author(s):  
S. E. Hill ◽  
W. J. V. Osterhout

Treatment of Nitella with distilled water apparently removes from the cell something which is responsible for the normal irritability and the potassium effect, (i.e. the large P.D. between a spot in contact with 0.01 M KCl and one in contact with 0.01 M NaCl). Presumably this substance (called R) is partially removed from the protoplasm by the distilled water. When this has happened a pinch which forces sap out into the protoplasm can restore its normal behavior. The treatment with distilled water which removes the potassium effect from the outer protoplasmic surface does not seem to affect the inner protoplasmic surface in the same way since the latter retains the outwardly directed potential which is apparently due to the potassium in the sap. But the inner surface appears to be affected in such fashion as to prevent the increase in its permeability which is necessary for the production of an action current. The pinch restores its normal behavior, presumably by forcing R from the sap into the protoplasm.


1936 ◽  
Vol 20 (1) ◽  
pp. 13-43 ◽  
Author(s):  
W. J. V. Osterhout

In normal cells of Valonia the order of the apparent mobilities of the ions in the non-aqueous protoplasmic surface is K > Cl > Na. After treatment with 0.01 M guaiacol (which does not injure the cell) the order becomes Na > Cl > K. As it does not seem probable that such a reversal could occur with simple ions we may assume provisionally that in the protoplasmic surface we have to do with charged complexes of the type (KXI)+, (KXII)+, where XI and XII are elements or radicals, or with chemical compounds formed in the protoplasm. When 0.01 M guaiacol is added to sea water or to 0.6 M NaCl (both at pH 6.4, where the concentration of the guaiacol ion is negligible) the P.D. of the cell changes (after a short latent period) from about 10 mv. negative to about 28 mv. positive and then slowly returns approximately to its original value (Fig. 1, p. 14). This appears to depend chiefly on changes in the apparent mobilities of organic ions in the protoplasm. The protoplasmic surface is capable of so much change that it does not seem probable that it is a monomolecular layer. It does not behave like a collodion nor a protein film since the apparent mobility of Na+ can increase while that of K+ is decreasing under the influence of guaiacol.


1944 ◽  
Vol 28 (1) ◽  
pp. 23-36 ◽  
Author(s):  
W. J. V. Osterhout

When protoplasm dies it becomes completely and irreversibly permeable and this may be used as a criterion of death. On this basis we may say that when 0.2 M formaldehyde plus 0.001 M NaCl is applied to Nitella death arrives sooner at the inner protoplasmic surface than at the outer. If, however, we apply 0.17 M formaldehyde plus 0.01 M KCl death arrives sooner at the outer protoplasmic surface. The difference appears to be due largely to the conditions at the two surfaces. With 0.2 M formaldehyde plus 0.001 M NaCl the inner surface is subject to a greater electrical pressure than the outer and is in contact with a higher concentration of KCl. In the other case these conditions are more nearly equal so that the layer first reached by the reagent is the first to become permeable. The outer protoplasmic surface has the ability to distinguish electrically between K+ and Na+ (potassium effect). Under the influence of formaldehyde this ability is lost. This is chiefly due to a falling off in the partition coefficient of KCl in the outer protoplasmic surface. At about the same time the inner protoplasmic surface becomes completely permeable. But the outer protoplasmic surface retains its ability to distinguish electrically between different concentrations of the same salt, showing that it has not become completely permeable. After the potential has disappeared the turgidity (hydrostatic pressure inside the cell) persists for some time, probably because the outer protoplasmic surface has not become completely permeable.


1933 ◽  
Vol 17 (1) ◽  
pp. 105-108 ◽  
Author(s):  
W. J. V. Osterhout ◽  
S. E. Hill

Not only does distilled water take away the irritability of Nitella but it also changes its behavior toward potassium. In normal cells potassium is strongly negative to sodium but after sufficient exposure to distilled water this effect disappears. It can be restored by returning the cells to their normal environment or to a suitable nutrient solution. This change in the protoplasm seems to be chiefly in its outer surface.


1945 ◽  
Vol 29 (1) ◽  
pp. 43-56 ◽  
Author(s):  
W. J. V. Osterhout

Remarkable changes are brought about by KOH in transforming negative cells of Nitella (showing dilute solution negative with KOH) to positive cells (showing dilute solution positive with KOH). NaOH is less effective as a transforming agent. This might be explained on the ground that the protoplasm contains an acid (possibly a fatty acid) which makes the cell negative and which is dissolved out more rapidly by KOH than by NaOH, as happens with the fatty acids in ordinary soaps. Part of a negative cell can be changed to positive by exposure to KOH while the untreated portion remains negative. After exposure to KOH the potential the protoplasm has when in contact with NaCl may increase. At the same time there may be an increase in the potassium effect; i.e., in the change of P.D. in a positive direction observed when 0.01 M KCl is replaced by 0.01 M NaCl. In some cases the order of ionic mobilities is uK > vOH > uNa. This shows that the protoplasmic surface cannot be a pore system: for in such a system all cations must have greater mobilities than all anions or vice versa.


1942 ◽  
Vol 25 (6) ◽  
pp. 905-916 ◽  
Author(s):  
L. R. Blinks

The effect of temperature upon the bioelectric potential across the protoplasm of impaled Valonia cells is described. Over the ordinary tolerated range, the P.D. is lowest around 25°C., rising both toward 15° and 35°. The time curves are characteristic also. The magnitude of the temperature effect can be controlled by changing the KCl content of the sea water (normally 0.012 M): the magnitude is greatly reduced at 0.006 M KCl, enhanced at 0.024 M, and greatly exaggerated at 0.1 M KCl. Conversely, temperature controls the magnitude of the potassium effect, which is smallest at 25°, with a cusped time course. It is increased, with a smoothly rising course, at 15°, and considerably enhanced, with only a small cusp, at 35°. A temporary "alteration" of the protoplasmic surface by the potassium is suggested to account for the time courses. This alteration does not occur at 15°; the protoplasm recovers only slowly and incompletely at 25°, but rapidly at 35°, in such fashion as to make the P.D. more negative than at 15°. This would account for the temperature effects observed in ordinary sea water.


Bact. lactis aerogenes first subcultured into D-arabinose has a long lag phase, in one strain about 30 hr. This is shown by cultures freshly grown from a single colony, and is not significantly changed by repeated subculture in a variety of media free from D-arabinose. According, therefore, to the theory that mutations and reverse mutations lead to an equilibrium and that the lag is the time required for the small proportion of mutants to multiply in the D-arabinose, this proportion must be very small, and the equilibrium rapidly established. Differential equations can be set up to express the rate of establishment of equilibrium starting either with normal cells (not utilizing D-arabinose) or with mutant cells. From the experimental observations an estimate can be made of the minimum rate of establishment of equilibrium in the forward direction, and the equations then can be applied to calculate the rate at which reverse mutation should occur. The calculations can be compared with the experimental results on the stability of D-arabinose adaptation during subsequent culture of the mutant cells in glucose. Reversion does not occur in the predicted manner. The theory would also fail to account for the generally observed influence of the length of training of bacteria on the ease of reversion. Theories of direct adaptation do not present these difficulties (though they do not themselves make any general prediction about the rate of reversion).


2017 ◽  
Vol 114 (21) ◽  
pp. 5337-5342 ◽  
Author(s):  
Xinyu Tian ◽  
Bo Huang ◽  
Xiao-Peng Zhang ◽  
Mingyang Lu ◽  
Feng Liu ◽  
...  

Intrinsic tumor-suppressive mechanisms protect normal cells against aberrant proliferation. Although cellular signaling pathways engaged in tumor repression have been largely identified, how they are orchestrated to fulfill their function still remains elusive. Here, we built a tumor-suppressive network model composed of three modules responsible for the regulation of cell proliferation, activation of p53, and induction of apoptosis. Numerical simulations show a rich repertoire of network dynamics when normal cells are subject to serum stimulation and adenovirus E1A overexpression. We showed that oncogenic signaling induces ARF and that ARF further promotes p53 activation to inhibit proliferation. Mitogenic signaling activates E2F activators and promotes Akt activation. p53 and E2F1 cooperate to induce apoptosis, whereas Akt phosphorylates p21 to repress caspase activation. These prosurvival and proapoptotic signals compete to dictate the cell fate of proliferation, cell-cycle arrest, or apoptosis. The cellular outcome is also impacted by the kinetic mode (ultrasensitivity or bistability) of p53. When cells are exposed to serum deprivation and recovery under fixed E1A, the shortest starvation time required for apoptosis induction depends on the terminal serum concentration, which was interpreted in terms of the dynamics of caspase-3 activation and cytochrome c release. We discovered that caspase-3 can be maintained active at high serum concentrations and that E1A overexpression sensitizes serum-starved cells to apoptosis. This work elucidates the roles of tumor repressors and prosurvival factors in tumor repression based on a dynamic network analysis and provides a framework for quantitatively exploring tumor-suppressive mechanisms.


1943 ◽  
Vol 27 (2) ◽  
pp. 91-100 ◽  
Author(s):  
W. J. V. Osterhout

The protoplasm of certain cells is able to distinguish electrically between K+ and Na+. This has been called the potassium effect. This is illustrated by experiments with Nitella. When 0.01 M KCl which has stood in contact with Nitella is replaced by 0.01 M NaCl the P.D. changes in a positive direction by an amount which varies between 30 and 95 mv. This ability to distinguish between K+ and Na+ disappears with the removal of an organic substance from the cell. The amount of this substance is doubtless too small to make it possible to obtain enough for analysis. An attempt has therefore been made to find an organic compound which can produce similar effects. It is found that when M/1 KCl in contact with nitrobenzene (previously shaken with M/1 KCl) is replaced by M/1 NaCl the potential changes in a positive direction to the extent of 67 mv. which compares favorably with the values found in Nitella. This is not due to a greater mobility in nitrobenzene of K+ as compared with Na+: this is evident from measurements of concentration effects with nitrobenzene (M/1 KCl vs. M/10 KCl and M/1 NaCl vs. M/10 NaCl). It might be brought about if KCl produced in nitrobenzene a sufficient preponderance of ions (simple or complex) as compared with NaCl. Whether this occurs could not be determined but it was found that nitrobenzene shaken with M/1 KCl has a higher conductivity than when shaken with M/1 NaCl. Measurements with salicylates showed that K-salicylate has a partition coefficient about 11.7 times as great as that of Na-salicylate. It was also found that when M/1 K-salicylate in contact with nitrobenzene (previously shaken with M/1 K-salicylate) is replaced by M/1 Na-salicylate there is a change of potential in a positive direction amounting to 56 mv. To what extent phase boundary potentials may enter into the observed values cannot be determined at present. The model resembles the Nitella cell in that RbCl and KCl are negative to NH4Cl which in turn is negative to NaCl and still more so to LiCl (in the model CsCl is negative to KCl but in Nitella it is positive). It likewise resembles Nitella in that the potassium effect is lessened by the addition of guaiacol.


2003 ◽  
Vol 50 (1) ◽  
pp. 191-195 ◽  
Author(s):  
Janusz Blasiak ◽  
Kinga Widera ◽  
Tomasz Pertyński

Hyperthermia can modulate the action of many anticancer drugs, and DNA repair processes are temperature-dependent, but the character of this dependence in cancer and normal cells is largely unknown. This subject seems to be worth studying, because hyperthermia can assist cancer therapy. A 1-h incubation at 37 degrees C of normal human peripheral blood lymphocytes and human myelogenous leukemia cell line K562 with 0.5 microM doxorubicin gave significant level of DNA damage as assessed by the alkaline comet assay. The cells were then incubated in doxorubicin-free repair medium at 37 degrees C or 41 degrees C. The lymphocytes incubated at 37 degrees C needed about 60 min to remove completely the damage to their DNA, whereas at 41 degrees C the time required for complete repair was shortened to 30 min. There was also a difference between the repair kinetics at 37 degrees C and 41 degrees C in cancer cells. Moreover, the kinetics were different in doxorubicin-sensitive and resistant cells. Therefore, hyperthermia may significantly affect the kinetics of DNA repair in drug-treated cells, but the magnitude of the effect may be different in normal and cancer cells. These features may be exploited in cancer chemotherapy to increase the effectiveness of the treatment and reduce unwanted effects of anticancer drugs in normal cells and fight DNA repair-based drug resistance of cancer cells.


Sign in / Sign up

Export Citation Format

Share Document