The hydrated potassium complex of the ionophore monensin A

1987 ◽  
Vol 109 (7) ◽  
pp. 2163-2165 ◽  
Author(s):  
Walter Pangborn ◽  
William Duax ◽  
David Langs
ChemInform ◽  
1987 ◽  
Vol 18 (33) ◽  
Author(s):  
W. PANGBORN ◽  
W. DUAX ◽  
D. LANGS

2006 ◽  
Vol 25 (5) ◽  
pp. 349-359 ◽  
Author(s):  
Seemha Bharadwaj ◽  
Shailendra Singh Rathore ◽  
Prahlad C. Ghosh

Ricin was encapsulated in negatively charged liposomes and its effect on the cytotoxicity was compared with native ricin in Chinese hamster ovarian (CHO) cells. The cytotoxicity of ricin, as measured by a marker protein synthesis (incorporation of 3H-leucine), was reduced markedly (300-fold) following encapsulation in liposomes. Lactose, a potent inhibitor of ricin cytotoxicity, had no effect on the binding, internalization, and cytotoxicity of liposomal ricin, indicating that liposomal ricin enter into mammalian cells by an alternative route, bypassing galactose-mediated endocytic pathway. Both monensin (a carboxylic ionophore) and NH4Cl (a lysosomotropic amine) markedly enhances the cytotoxicity of liposomal ricin, indicating endocytotic uptake of liposomal ricin. The degree of potentiation of the cytotoxicity of liposomal ricin by both monensin and NH4Cl was significantly higher (441- and 51-fold) as compared to native ricin (62.5- and 12.5-fold). The extent of exocytosis of free ricin was found to be much higher as compared to liposomal ricin; on the other hand, the extent of degradation of free and liposomal ricin was identical. Consequently, the intracellular level of liposomal ricin was increased to 3.5-fold. This higher level of intracellular liposomal ricin may allow more efficient ricin A-chain release into the cytosol under the influence of NH4Cl and monensin. Monensin-induced potentiation of liposomal ricin was prevented by brefeldin A, indicating that in the presence of monensin, the liposomal ricin was efficiently routed through the Golgi apparatus en route to the cytosol. Thus, liposomal ricin in combination with monensin may have potential application for selective elimination of malignant cells.


2018 ◽  
Vol 92 (2) ◽  
pp. 1537-1546 ◽  
Author(s):  
Greta Klejborowska ◽  
Ewa Maj ◽  
Joanna Wietrzyk ◽  
Joanna Stefańska ◽  
Adam Huczyński

1982 ◽  
Vol 70 (5) ◽  
pp. 1074-1080 ◽  
Author(s):  
M R Clark ◽  
N Mohandas ◽  
S B Shohet

2007 ◽  
Vol 832 (1-3) ◽  
pp. 84-89 ◽  
Author(s):  
Adam Huczyński ◽  
Małgorzata Ratajczak-Sitarz ◽  
Andrzej Katrusiak ◽  
Bogumil Brzezinski

1986 ◽  
Vol 250 (4) ◽  
pp. H612-H619 ◽  
Author(s):  
R. S. Moreland ◽  
T. C. Major ◽  
R. C. Webb

This study characterizes isometric force development in response to ouabain and K+-free solution in isolated aortic strips from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. SHR aortas were more sensitive to ouabain than those from WKY (threshold: SHR, 3.1 X 10(-5) M; WKY, 25.6 X 10(-5) M), and force development in response to 10(-3) M ouabain was greater in SHR (SHR, 586 +/- 51 mg; WKY, 245 +/- 24 mg). Monensin, a Na+ ionophore, potentiated contractile responses to ouabain, whereas amiloride, a Na+ channel blocker, and low Na+ solutions depressed contractile responses to ouabain. Contractile responses of SHR aortic strips to K+-free solution were faster than those of WKY aortic strips [time to half-maximal response (t1/2): SHR, 24 +/- 5 min; WKY, 47 +/- 4 min]. Maximal force development by aortic strips from SHR in response to K+-free solution was not different from that of WKY aortic strips (SHR, 808 +/- 34 mg; WKY, 750 +/- 37 mg). Monensin (10(-5) M) increased the rate of force development to K+-free solution to a greater extent in WKY aortic strips than in those from SHR (t1/2: SHR, 3 +/- 1 min; WKY, 4 +/- 2 min). Amiloride and low Na+ solution depressed contractile responses to K+-free solution in both SHR and WKY aortic strips. These observations demonstrate that SHR aortas are more responsive to ouabain and K+-free solution compared with WKY aortas. Contractile responses to ouabain and K+-free solution were sensitive to experimental interventions that alter transmembrane Na+ movements.(ABSTRACT TRUNCATED AT 250 WORDS)


1984 ◽  
Vol 100 (3-4) ◽  
pp. 299-307 ◽  
Author(s):  
H. Ozaki ◽  
T. Kishimoto ◽  
S. Chihara ◽  
H. Umeno ◽  
N. Urakawa

1974 ◽  
Vol 3 (1) ◽  
pp. 25-35 ◽  
Author(s):  
M.L. Clarke ◽  
M. Diaz ◽  
B. Guilloteau ◽  
P.L Hudd ◽  
J.W. Stoker

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