Vinleurosine
Vinleurosine can partially inhibit the energy dependent transport of alpha-aminoisobutyric acid in Ehrlich ascites tumor cells.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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J Cell Physiol. 1975 Oct;86(2 Pt 1):201-11.
A reduction in energy-dependent amino acid transport by microtubular inhibitors in Ehrlich ascites tumor cells.[Pubmed:
1194361]
Vincristine, other periwinkle alkaloids, and colchicine partially inhibit the energy dependent transport of alpha-aminoisobutyric acid in Ehrlich ascites tumor cells. The properties of this phenomenon were characterized in detail for vincristine. Maximum depression of the steady-state intracellular alpha-aminoisobutyric acid level was achieved with a vincristine concentration of less than 0.5 muM. The inhibitory effect of vincristine increases as the extracellular alpha-aminoisobutyric acid concentration is increased reaching a maximum, however, of only approximately to 25% at a level of 5 mM, leaving a large gradient for alpha-aminoisobutyric acid across the cell membrane. Vincristine produced an asymmetrical uptake rate, while increasing the efflux of alpha-aminoisobutyric acid. Inhibition of net alpha-aminoisobutyric acid transport by vincristine was partially reversible (approximately to 40%). Colchicine (50 muM) reduced the steady-state alpha-aminoisobutyric acid level by 30%, an effect that was not reversible. Inhibition by Vinleurosine and vinrosidine was comparable to that of vincristine. Addition of glucose to the medium resulted in a small, but significant, decrease in the inhibitory effects of both vincristine and colchicine. The data indicate that these agents inhibit a small component of the uphill transport of alpha-aminoisobutyric acid in Ehrlich ascites tumor cells. The inhibitory effect of vincristine cannot be attributed to an increase in the passive permeability of the cell membrane to this agent. Rather, the data along with other studies from this laboratory suggest that vincristine reduces the energy-dependent transport of alpha-aminoisobutyric acid by either inhibiting cellular energy metabolism or by inhibiting cellular energy metabolism or by inhibiting the coupling of energy-metabolism to the transport of this amino acid and raises the possibility that cellular microtubules play a role in these processes.
