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The most abundant green tea polyphenol, epigallocatechin-3-gallate (EGCG), was found to induce differential effects between tumor cells and normal cells. Nevertheless, how normal epithelial cells respond to the polyphenol at concentrations for which tumor cells undergo apoptosis is undefined. The current study tested exponentially growing and aged primary human epidermal keratinocytes in response to EGCG or a mixture of the four major green tea polyphenols. EGCG elicited cell differentiation with associated induction of p57/KIP2 within 24 h in growing keratinocytes, measured by the expression of keratin 1, filaggrin, and transglutaminase activity. Aged keratinocytes, which exhibited low basal cellular activities after culturing in growth medium for up to 25 days, renewed DNA synthesis and activated succinate dehydrogenase up to 37-fold upon exposure to either EGCG or the polyphenols. These results suggest that tea polyphenols may be used for treatment of wounds or certain skin conditions characterized by altered cellular activities or metabolism.Green tea polyphenols (referred to as GTPPs, to include the four major polyphenols: epicatechin, epigallocatechin, epcatechin-3-gallate, and epigallocatechin-3-gallate (EGCG) have been identified to possess chemopreventive and apoptotic activity against certain cancers, whereas normal epidermal keratinocytes follow a survival pathway that has not been fully elucidated (Chen et al

Green tea polyphenols (GTPPs) are considered beneficial to human health, especially as chemopreventive agents. Recently, cytotoxic reactive oxygen species (ROS) were identified in tumor and certain normal cell cultures incubated with high concentrations of the most abundant GTPP, (Ϫ)-epigallocatechin-3-gallate (EGCG). If EGCG also provokes the production of ROS in normal epithelial cells, it may preclude the topical use of EGCG at higher doses. The current study examined the oxidative status of normal epithelial, normal salivary gland, and oral carcinoma cells treated with EGCG, using ROS measurement and catalase and superoxide dismutase activity assays. The results demonstrated that high concentrations of EGCG induced oxidative stress only in tumor cells. In contrast, EGCG reduced ROS in normal cells to background levels. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and 5-bromodeoxyuridine incorporation data were also compared between the two oral carcinoma cell lines treated by EGCG, which suggest that a difference in the levels of endogenous catalase activity may play an important role in reducing oxidative stress provoked by EGCG in tumor cells. It is concluded that pathways activated by GTPPs or EGCG in normal epithelial versus tumor cells create different oxidative environments, favoring either normal cell survival or tumor cell destruction. This finding may lead to applications of naturally occurring polyphenols to enhance the effectiveness of chemo/radiation therapy to promote cancer cell death while protecting normal cells.

Previous studies of the effects of nicotine on fibroblasts have reported an altered morphology and attachment of fibroblasts to substrates and disturbances in protein synthesis and secretion. This altered functional and attachment response may be associated with changes in the cell membrane resulting from binding of the nicotine, or to disturbances in cell metabolism as a result of high intracellular levels of nicotine. The purpose of the present study, therefore, was to 1) determine whether gingival fibroblasts bound nicotine and if any binding observed was specific or non‐specific in nature; 2) determine whether gingival fibroblasts internalized nicotine, and if so, at what rate; 3) determine whether gingival fibroblasts also released nicotine back into the extracellular environment; and 4) if gingival fibroblasts release nicotine intact or as a metabolite. Cultures of gingival fibroblasts were prepared from gingival connective tissue biopsies. Binding was evaluated at 4° C using a mixture of 3H‐nicotine and unlabeled nicotine. Specific binding was calculated as the difference between 3H‐nicotine bound in the presence and absence of unlabeled nicotine. The cells bound 1.44 (± 0.42) pmols/106 cells in the presence of unlabeled nicotine and 1.66 (± 0.55) pmols/106 cells in the absence of unlabeled nicotine. The difference was not significant. Uptake of nicotine was measured at 37° C after treating cells with 3H‐nicotine for time periods up to 4 hours. Uptake in pmols/106 cells was 4.90 (± 0.34) at 15 minutes, 8.30 (± 0.75) at 30 minutes, 12.28 (± 2.62) at 1 hour and 26.31 (± 1.15) at 4 hours. The efflux or release of nicotine was evaluated after treating cells with 3H‐nicotine for 4 hours and then measuring the amount of 3H‐nicotine released into fresh non‐radioactive medium over a 2‐hour period by direct scintillation counting of aliquots of medium and by chromatographic analysis of medium samples. Cells released nicotine back into the medium at a rate much slower than the rate of uptake, and the majority of nicotine released by the cells over the 2‐hour period was in the form of nicotine rather than a metabolite. At earlier time points, a greater percentage of the 3H isotope separated chromatographically before 3H‐nicotine, suggesting an association of the nicotine with intracellular vesicles or other intracellular components. The results of this study suggest that, although nicotine does bind to gingival fibroblasts, this binding is non‐specific, and that the uptake of nicotine by these cells is continuous over 4 hours, providing high intracellular levels. In addition, gingival fibroblasts also release nicotine, apparently unmetabolized, back into the medium. However, an apparent association of the nicotine with intracellular components seems to result in the development of high intracellular levels of nicotine which may interfere with normal cellular functions. J Periodontol 1991; 62:147‐152.

Physical property enhancement in light-cured resin composites from post-cure heating is attributed to free radicals created during initial photocuring, the number of which decreases following initial light-curing. Clinically, it is important to know when the number of remaining free radicals is too low to provide for additional conversion of monomer in post-cure-heated specimens. The hypothesis tested is that the potential for additional conversion in post-cure-heated resin composite restorations is dependent upon the time after initial light-curing at which the specimen is exposed to heat treatment. This research examined the effect of delay in post-cure heating after initial photo-activation on strength and monomer conversion of a commercial resin composite material. Discs (10 x 1 mm) of Herculite XRV (Kerr/Sybron, Orange, CA) were photocured at standardized conditions. One group was left unheated, and another was subjected to post-cure heating (Brilliant DI-500, Coltène AG, Altstätten, Switzerland) at the following times after being light-cured: 5 and 30 min, and 6, 24, 48, 72, 96, and 120 hrs. After the appropriate delay time, unheated and heated specimens (n = 10) were tested for biaxial flexural strength at a constant stressing rate. Recovered, fractured strength specimens (n = 10) were analyzed for cure by means of IR spectroscopy. Post-cure heating increased strength over that of the unheated specimens only for the shortest delay times: 5 or 30 min. Thereafter, strength values were statistically equivalent (p < 0.05). Delay in heating did not significantly enhance strength of post-cure-heated specimens, but delay in time did improve strength of the unheated groups. The greatest monomer conversion was obtained when post-cure heating was applied within 6 hrs following light-curing. The difference in cure between unheated and heated specimens remained significant up to 96 hrs of delay. Flexural strength of post-cure-heated specimens remained unchanged with time delay for heating specimens. Maximal monomer conversion of post-cured specimens is obtained only within 6 hrs of light-curing. The potential for additional conversion arising from post-cure heat treatment is dependent upon the time following initial curing at which heat is applied following initial light-curing. However, delay in heat application has no influence on flexural strength.