Decrease in the antioxidant capacity in beverages containing tea extracts during storage.

The aim of this work was to determine antioxidant capacity of beverages containing black, white, and green tea extracts using the photochemiluminescence method, and to monitor its changes based on the storage temperature and time. Samples were stored at two different temperatures (refrigerated at 4°C and laboratory temperature 22°C), analyzed after opening of the original package, and consequently after 4 and 7 days. Results of the antioxidant capacity are expressed as the standard equivalents, that is, ascorbic acid in mmol/L. The highest mean value of the antioxidant capacity was found after opening of the original package in fruit-juice-enriched samples and totaled 9.793 mmol/L. This group revealed significant dependence (P < 0.05) not only on the storage time, but also temperature. In samples without added fruit juices containing preservatives the value was 0.428 mmol/L. This group showed significant dependence (P < 0.05) on the decrease of antioxidant capacity only when based on the storage time. Samples without fruit juices or preservatives showed significant decrease in the antioxidant capacity (P < 0.05) after 4 days of storage based on the storage time. The dependence on temperature was revealed only after 7 days of storage.

Interferon-gamma, but not interferon-alpha, induces SOCS 3 expression in human melanoma cell lines.

The signal transducers and transcription activators (STATs) and their endogenous inhibitors of the suppressors of cytokine signalling (SOCS) family are major proteins harmonizing the transmission of external signals from the surface membrane to target genes in the nucleus. To correlate the induction of SOCS 3 by interferons (IFNs) on messenger RNA and protein levels with STAT 1 phosphorylation in human malignant melanoma cell lines, we used a unique collection of 18 established malignant melanoma cell lines and six human non-malignant normal cells (two melanocytes, two skin keratinocytes and two fibroblasts). IFN-gamma induced SOCS 3 in 83% of melanoma cell lines, whereas IFN-alpha stimulated SOCS 3 expression in only 11% of cases. Similarly, melanocytes showed strong induction of SOCS 3 by IFN-gamma and, to a lesser extent, by IFN-alpha. In most cases, SOCS 3 expression was paralleled by STAT 1 phosphorylation at tyrosine residues (Y701). In several lines, however, SOCS 3 was not induced despite STAT 1 phosphorylation and, in a few lines, SOCS 3 induction occurred without detectable STAT 1 phosphorylation, indicating that STAT 1 might not be an exclusive inducer of SOCS 3. Similarly, non-malignant cells displayed STAT 1 activation and high levels of SOCS 3 expression after IFN-gamma (but not IFN-alpha) treatment. In conclusion, in contrast to IFN-alpha, IFN-gamma appeared to induce SOCS 3 apparently at the transcription level and exhibited higher cytotoxic effects regardless of the cell origin.

Src tyrosine kinase but not activated Ras augments sensitivity to taxanes through apoptosis in human adenocarcinoma cells.

We investigated the mechanistic role of Src and Ras, important oncoproteins implicated in the pathogenesis of many human cancers, in taxane-induced apoptosis using v-src or c-H-ras transfected HAG-1 human gallbladder epithelial cells. Compared with the parental HAG-1 cell line, v-src-transfected HAG/src3-1 cells became 6.0-fold and 7.5-fold sensitive to taxotere, and 1.8-fold and 3.9-fold sensitive to taxol, for 2-hour and 24-hour exposures, respectively. By contrast, HAG-1 cells transfected with activated Ras, which acts downstream of Src, acquired approximately 2.7- and 5.0-fold taxotere resistance, and 2.3- and 2.8-fold taxol resistance, for both exposures, respectively. To examine the mechanism(s) whereby Src augments sensitivity to taxanes, we investigated the functional role of Src in taxotere-induced apoptosis. Treatment of HAG/src3-1 cells with taxotere resulted in subsequent induction of apoptotic cell death, whereas apoptosis did not occur in parental or c-H-ras-transfected HAG/ras5-1 cells. Moreover, a protein kinase C (PKC) and a phosphatidylinositol-3 kinase (PI-3 kinase) inhibitors (H-7 and wortmannin, respectively) did not alter either taxotere sensitivity or taxotere-induced apoptosis in these cells. Similarly, non-cytotoxic concentrations of geldanamycin, which destabilizes c-Raf-1 kinase, did not prevent apoptosis in HAG/src3-1 cells. These data indicate that the ability of activated Src to sensitize HAG/src3-1 cells to taxotere might be mediated by apoptotic events occurring through Src to downstream signal transduction pathways, excluding activated Ras, Raf-1 kinase, PI-3 kinase and PKC.