Ammonium acetate decreased in a concentration-dependent manner the phagocytic uptake of mannosylated latex microspheres and of yeast by immortalized human microglia (CHME-5) and astroglioma (GL-15) cells. In both cell lines ammonium acetate affected also the secretion of certain cytokines. The most conspicuous effects were the following: in both cell lines ammonium acetate enhanced greatly the secretion of tumor necrosis factor-alpha in the absence of any other stimulus. in the human microglia cells ammonia decreased the constitutive secretion of interleukin-6, but it enhanced the stimulated (interleukin-1 alpha, tumor necrosis factor-alpha, gamma-interferon and gamma-interferon + tumor necrosis factor-alpha) secretion of interleukin-8. In the astroglioma cell line, the stimulated release of tumor necrosis factor-alpha, interleukin-6 and interleukin-8 was diminished by ammonium acetate. The magnitude of the ammonia-effect depended on the stimulating agent (lipopolysaccharide, interleukin-1 alpha, tumor necrosis factor-alpha, gamma-interferon). The results are discussed with regard to their potential importance in the pathogenesis of human diseases with elevated blood and brain ammonia concentrations.

Acetates↗

PubMedDate not supplied

Characterisation of taurine uptake in human KB MDR and non-MDR tumour cell lines in culture.

Studies on taurine transport in MDR (multidrug resistant) and non-MDR KB cancer cells show that both cell types contain Na(+)- and Cl(-)-dependent high-affinity and low-affinity transport systems selective for beta-amino acids and a taurine diffusion component. Good buffers, such as HEPES or MOPS, interfered with taurine uptake. The basal taurine Vmax measured in isoosmotic medium represented 1/5 of taurine captured by uptake in KB non-MDR, but was negligible in KB MDR cells. High-and low- affinity uptake systems were reduced by medium hyperosmolarity in both cell types. Although properties of low-and high-affinity transport systems were similar in both cell types, Vmax (but not Km) were reduced in MDR compared to non-MDR cells. Taurine uptake was unaffected by chemotherapeutic agents (doxorubicin, vinblastine) or MDR revertants (verapamil). Taurine did not affect cell proliferation of MDR or non-MDR cells nor did it alter the inhibitory effect of doxorubicin or vinblastine cell proliferation.

Buffers↗

PubMedDate not supplied

Enhanced sialylation of the K 562 cell surface membrane glycoconjugates induced by adriamycin.

The antitumor agent Adriamycin (ADM) increases the sialic acid content of K 562 cell plasma membrane glycoconjugates. Total and neuraminidase-sensitive sialic acid are enhanced 3 to 4 times when expressed per 10(6) cells. This fact is a consequence of an increase in cell surface and in plasma membrane sialic acid density. Protein-bound and lipid-bound sialic acid are increased in the same way and exhibit the same ratio 90/10. After external radiolabelling by periodide-borotritide and neuraminidase-galactose oxidase-borotritide treatment, only some quantitative changes can be observed. Fractionation of gangliosides by thin layer chromatography gives the same results. Further experiments lead to the following conclusions: the hypersialylation cannot be explained by a G2-block in the cell cycle induced by ADM; it is not a consequence of a differentiation process; it is not observed in a population of adriamycin-resistant K 562 cells and can therefore be considered as a metabolic event linked to the cytotoxic activity of ADM.

Cell Cycle↗