An evaluation of microbiologic contamination on phosphor plates in a dental school.

OBJECTIVE: The objective of this study was to determine if phosphor plates used in predoctoral clinics are microbiologically contaminated and to identify the source of contamination. STUDY DESIGN: Forty-five of 300 phosphor plates (15%) were randomly selected for examination. The plates were pressed into individual blood agar plates, were incubated using standard techniques at 37 degrees C, and were monitored for 72 hours. The number, size, distribution, and variety of resulting colonies were noted. A representative of each type of colony was selected to be Gram stained using the standard technique. RESULTS: Of the plates, 42.2% were uncontaminated, 57.8% yielded bacterial colonies, and 15.6% of those colonies demonstrated hemolytic growth. The hemolytic growth included combined alpha and beta hemolysis and beta only hemolysis. Six colonies were gram-positive rods and 7 were gram-positive cocci. CONCLUSION: Meticulous infection-control techniques are inevitable and continuous reinforcement and training for staff and students are mandatory. Periodic gas sterilization of phosphor plates may be necessary.

Effects of oral consumption of the green tea polyphenol EGCG in a murine model for human Sjogren's syndrome, an autoimmune disease.

SIGNIFICANCE: Protection of glandular cells from autoimmune-induced damage would be of significant clinical benefit to Sjogren's syndrome (SS) patients. Epigallocatechin-3-gallate (EGCG) possesses anti-apoptotic, anti-inflammatory, and autoantigen-inhibitory properties. AIMS: To investigate if EGCG protects against certain autoimmune-induced pathological changes in the salivary glands of the non-obese diabetic (NOD) mouse model for SS. MAIN METHODS: Animals were provided with either water or water containing 0.2% EGCG. At the age of 8, 16 and 22 weeks, submandibular salivary gland tissue and serum samples were collected for pathological and serological analysis. KEY FINDINGS: Significant lymphocyte infiltration was observed in the salivary glands of the water-fed group at the age of 16 weeks, while the EGCG group showed reduced lymphocyte infiltration. By 22 weeks of age, water-fed animals demonstrated elevated levels of apoptotic activity within the lymphocytic infiltrates, and high levels of serum total anti-nuclear antibody, compared to EGCG-fed animals. Remarkably, proliferating cell nuclear antigen (PCNA) and Ki-67 levels in the salivary glands of water-fed NOD mice were significantly elevated in comparison to BALB/c control mice; in contrast, PCNA and Ki-67 levels in EGCG-fed NOD animals were similar to BALB/c mice. These results indicate that EGCG protects the NOD mouse submandibular glands from autoimmune-induced inflammation, and reduces serum autoantibody levels. Abnormal proliferation, rather than apoptosis, appears to be a characteristic of the NOD mouse gland that is normalized by EGCG. The evidence suggests that EGCG could be useful in delaying or managing SS-like autoimmune disorders.

Influence of matrix-suspended demineralized bone on osseous repair using a critical-sized defect in the rat (Rattus norvegicus) calvarium.

Demineralized freeze-dried bone (DFDB) in matrix form must be rehydrated with a carrier medium which allows for easy manipulation during periodontal surgery. The purpose of this study was to evaluate how human DFDB suspended in a polyol matrix affects new bone formation in the rat calvarium critical-sized defect (CSD) model. Fifty-five adult male Harlan Sprague-Dawley rats were assigned to 1 of 5 treatment groups: polyol, 100% DFDB, 47% DFDB/polyol, 47% DFDB, or an unfilled control. They were then placed into 8-m calvarial CSDs. The bone donor source company for the DFDB and DFDB/polyol groups was the same. Calvaria were harvested 10 weeks after surgery and evaluated histomorphometrically. The diameter of bone particles from the 3 groups containing DFDB was measured by scanning electron microscopy. There was no statistically significant difference in the percentage of bone fill between any of the groups, although the 100% DFDB group exhibited the most bone fill. The 47% DFDB/polyol and 47% DFDB groups had similar amounts of bone formation. The average size of the demineralized bone particles from the 100% DFDB group was significantly smaller than that of the other 2 groups containing DFDB. Adding a polyol to DFDB produced similar osseous regeneration in the rat calvarium defect model vs DFDB alone. Yet from a clinical standpoint, the polyol enhanced graft handling and stability. Graft particle size may have an effect on bone fill.

Green tea polyphenol induces caspase 14 in epidermal keratinocytes via MAPK pathways and reduces psoriasiform lesions in the flaky skin mouse model.

Psoriasiform lesions are characterized by hyperproliferation and aberrant differentiation of epidermal keratinocytes, accompanied by inflammation, leading to a disrupted skin barrier with an abnormal stratum corneum. The expression and proteolytic processing of caspase 14, a member of the caspase family which is associated with epithelial cell differentiation, planned cell death, and barrier formation, is altered in psoriatic epidermis. We recently reported that human psoriatic tissues lack normal expression of caspase 14 [J Dermatol Sci37 (2005) 61], and caspase 14 is induced by EGCG, a green tea polyphenol (GTP), in exponentially growing normal human epidermal keratinocytes (NHEK) [J Pharmacol Exp Ther315 (2005) 805]. This suggests that GTPs may have beneficial effects on psoriasiform lesions. The current study aimed to determine whether MAPK pathways are required for GTP-induced caspase 14 expression in NHEK and if GTPs can modulate the expression of pathological markers in the psoriasiform lesions that develop in the flaky skin mouse. The results indicate that the p38 and JNK MAPK pathways are required for EGCG-induced expression of caspase 14 in NHEK. Importantly, topical application of 0.5% GTPs significantly reduced the symptoms of epidermal pathology in the flaky skin mice, associated with efficient caspase 14 processing and reduction in proliferating cell nuclear antigen levels. This suggests that GTP-activated pathways may be potential targets for novel therapeutic approaches to the treatment of some psoriasiform skin disorders.

Expression of caspase-14 reduces tumorigenicity of skin cancer cells.

BACKGROUND: The green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) possesses anti-carcinogenic properties and was found to induce terminal differentiation in epidermal keratinocytes. Caspase-14, a member of the caspase family associated with epithelial cell differentiation, planned cell death, and barrier formation, is induced by EGCG in normal human epidermal keratinocytes but not in cancer cells. MATERIALS AND METHODS: A human epidermoid cancer cell line, A431, was co-transfected with a caspase-14-expressing pCMV vector and a GFP/neo-etpressingpCMVvector. Cell growth and tumorigenicity of the stable transfectant were determined in comparison to cells transfected with the control GFP/neo-expressing pCMV vector. RESULTS: Expression of exogenous caspase-14 led to growth inhibition and reduced the tumorigenicity of A431 cells. CONCLUSION: Pending future studies, caspase-14 could be used as a novel approach to skin cancer therapy via gene delivery systems.

Green tea polyphenols reduce autoimmune symptoms in a murine model for human Sjogren's syndrome and protect human salivary acinar cells from TNF-alpha-induced cytotoxicity.

Sjogren's syndrome (SS) is a relatively common autoimmune disorder. A key feature of SS is lymphocytic infiltration of the salivary and lacrimal glands, associated with the destruction of secretory functions of these glands. Current treatment of SS targets the symptoms but is unable to reduce or prevent the damage to the glands. We reported previously that the major green tea polyphenol (GTP) epigallocatechin-3-gallate (EGCG) inhibits autoantigen expression in normal human keratinocytes and immortalized normal human salivary acinar cells (Hsu et al. 2005). However, it is not known whether GTPs have this effect in vivo, if they can reduce lymphocytic infiltration, or protect salivary acinar cells from tumor necrosis factor-alpha (TNF-alpha)-induced cytotoxicity. Here, we demonstrate that in the NOD mouse, a model for human SS, oral administration of green tea extract reduced the serum total autoantibody levels and the autoimmune-induced lymphocytic infiltration of the submandibular glands. Further, we show that EGCG protected normal human salivary acinar cells from TNF-alpha-induced cytotoxicity. This protection was associated with specific phosphorylation of p38 MAPK, and inhibitors of the p38 MAPK pathway blocked the protective effect. In conclusion, GTPs may provide a degree of protection against autoimmune-induced tissue damage in SS, mediated in part through activation of MAPK elements.

Efficacy of two contemporary single-cone filling techniques in preventing bacterial leakage.

This in vitro study evaluated the sealing efficacy of three root-filling systems/techniques in preventing bacterial leakage. Instrumented single-rooted root segments were filled with (1) warm vertical compaction with gutta-percha/AH Plus; (2) single-cone technique with ActiV GP; and (3) single-cone technique with Gutta-Flow. A dual-chamber leakage model using S. mutans as a microbial marker was used for leakage evaluation. Bacterial penetration was monitored over a 100-day period. Leakage was recorded when turbidity was observed in the lower chamber. Gutta-percha warm vertical compaction exhibited the best seal with bacterial leakage observed in only 16.7% of the specimens between 59 and 100 days. All ActiV GP specimens leaked between 7 and 100 days; 50% of the Gutta-Flow specimens leaked between 22 and 100 days. The two contemporary single-cone techniques did not insure a durable apical seal against bacterial leakage. A warm vertical compaction technique using thermoplasticized gutta-percha and AH Plus sealer appears to be more effective in minimizing bacterial leakage.

EGCG-targeted p57/KIP2 reduces tumorigenicity of oral carcinoma cells: role of c-Jun N-terminal kinase.

The green tea polyphenol epigallocatechin-3-gallate (EGCG) regulates gene expression differentially in tumor and normal cells. In normal human primary epidermal keratinocytes (NHEK), one of the key mediators of EGCG action is p57/KIP2, a cyclin-dependent kinase (CDK) inhibitor. EGCG potently induces p57 in NHEK, but not in epithelial cancer cells. In humans, reduced expression of p57 often is associated with advanced tumors, and tumor cells with inactivated p57 undergo apoptosis when exposed to EGCG. The mechanism of p57 induction by EGCG is not well understood. Here, we show that in NHEK, EGCG-induces p57 via the p38 mitogen-activated protein kinase (MAPK) signaling pathway. In p57-negative tumor cells, JNK signaling mediates EGCG-induced apoptosis, and exogenous expression of p57 suppresses EGCG-induced apoptosis via inhibition of c-Jun N-terminal kinase (JNK). We also found that restoration of p57 expression in tumor cells significantly reduced tumorigenicity in athymic mice. These results suggest that p57 expression may be an useful indicator for the clinical course of cancers, and could be potentially useful as a target for cancer therapies.

Reduction in antimicrobial substantivity of MTAD after initial sodium hypochlorite irrigation.

Potential intrinsic tetracycline staining of intraradicular dentin has been observed when BioPure MTAD was employed as the final irrigant after initial rinsing with NaOCl. This study examined the effect of NaOCl-MTAD interaction on the antimicrobial substantivity of MTAD in dentin. Dentin cores previously irrigated with either MTAD, or in conjunction with 1.3% NaOCl as an initial irrigant were placed on blood agar plates inoculated with Escherichia faecalis at 10(5) cfu/ml. Dentin cores irrigated with 1.3% NaOCl only, and autoclaved dentin disks were used as the respective positive and negative controls. After anaerobic incubation, the mean diameter of bacterial inhibition zones formed around the MTAD group was significantly larger than the NaOCl/MTAD group, which, in turn, was not significantly different from the NaOCl positive control. Oxidation of MTAD by NaOCl resulted in the partial loss of antimicrobial substantivity in a manner similar to the peroxidation of tetracycline by reactive oxygen species.

Penetration of fluids into periodontal pockets using a powered toothbrush/irrigator device.

UNLABELLED: This study was a single-blind, randomized, controlled clinical trial. The researchers evaluated a powered brush/irrigating device (HydraBrush Oral Health System; OHS) for its safety and ability to deliver a solution to the bottom of 5-6 mm pockets, compared to rinsing alone with a solution following brushing with a powered toothbrush (Sonicare Elite 7800; SE). An evaluation technique to measure the quantity and quality of solution able to enter the pocket was also introduced in this project. METHODS: Subjects were randomized in one of two-groups: brush plus simultaneous irrigation (OHS) versus brush plus rinsing (SE). Subjects used their devices at home for two weeks. At the measurement visit, subjects used the OHS to irrigate and brush simultaneously for 1 minute (30 seconds per each side of the mouth) with a 0.01% erythrosine disclosing solution in 10 oz of distilled water. Control subjects brushed for 2 minutes with a SE followed by a 1 minute rinse with an identical disclosing solution. A blinded evaluator collected six samples of approximately of 1 microL of sucular fluid from six 5-6 mm evaluation sites. This was accomplished by inserting a microcapillary tip with a 20 microL micropipette in the sulcus. Two-group repeated measures ANOVA was used to examine differences in two measures of the disclosing solution between OHS and SE subjects; the spectrometer reading of the disclosing solutions, and by visual inspection of the samples (positive/negative) to determine the presence or absence of solution in the samples. Subjects' diaries were collected. Bleeding and discomfort during the evaluation period was reported. RESULTS: Visually, OHS had a significantly greater proportion of solution taken from the base of 5-6 mm sites than the SE (p=0.0001). However, there was no statistical difference between the two groups (p=.1359) in the spectrophotometer readings. CONCLUSION: The experimental device is more efficient in delivering a solution to the base of 5-6 mm pockets than rinsing following use of a control powered toothbrush. Both devices have demonstrated they are safe and well accepted by patients. The technique developed provides a useful method for quantitative and qualitative studies of solutions from the base of periodontal pockets.

Effects of sub-toxic concentrations of camphorquinone on cell lipid metabolism.

The biological effects of camphorquinone (CQ), an initiator for light-polymerized resins, have been reported to relate to its ability to generate free radicals and cause radical-induced membrane damage via lipid peroxidation. However, the effects of CQ on lipids other than peroxidation may result in unfavorable tissue responses especially at concentrations that are not overtly toxic to cells. The purpose of the current study was to examine the effects of CQ on cell lipid metabolism at subtoxic concentrations, with or without visible light irradiation. HCP and THP-1 cells were exposed to CQ with or without light irradiation under clinically relevant conditions and lipid metabolism was analyzed using 14C-labeling and thin-layer chromatography. We found that CQ increased synthesis of neutral lipids, such as triglycerides, from 7 to nearly 15% of the total and diglycerides from 2% to about 3% of the total in HCP cells, while synthesis of phospholipids, such as sphingomyelin, was decreased by 1-1.5%. In THP-1 cells cholesterol synthesis increased more than 2-fold and cholesterol ester synthesis increased more than 5-fold. Light-activated CQ did not differ significantly in terms of its bioactivity compared to no-light conditions. We conclude that CQ significantly altered the metabolism of several important structural lipids in two cell types at sub-toxic concentrations that are clinically relevant. These changes in lipid metabolism may in turn affect membrane integrity and permeability and possibly lead to significant changes in cell responses.

Inhibition of autoantigen expression by (-)-epigallocatechin-3-gallate (the major constituent of green tea) in normal human cells.

Autoimmune disorders, characterized by inflammation and apoptosis of target cells leading to tissue destruction, are mediated in part by autoantibodies against normal cellular components (autoantigens) that may be overexpressed. For example, antibodies against the autoantigens SS-A/Ro and SS-B/La are primary markers for systemic lupus erythematosus and Sjögren's syndrome. Recently, studies in animals demonstrated that green tea consumption may reduce the severity of some autoimmune disorders, but the mechanism is unclear. Herein, we sought to determine whether the most abundant green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), affects autoantigen expression in human cells. Cultures of pooled normal human primary epidermal keratinocytes and of an immortalized human salivary acinar cell line were incubated with 100 microM EGCG (a physiologically achievable level for topical application or oral administration) for various time periods and then analyzed by cDNA microarray analysis, reverse transcription-polymerase chain reaction, and Western blotting for expression of several major autoantigen candidates. EGCG inhibited the transcription and translation of major autoantigens, including SS-B/La, SS-A/Ro, coilin, DNA topoisomerase I, and alpha-fodrin. These findings, taken together with green tea's anti-inflammatory and antiapoptotic effects, suggest that green tea polyphenols could serve as an important component in novel approaches to combat autoimmune disorders in humans.

Role of p21WAF1 in green tea polyphenol-induced growth arrest and apoptosis of oral carcinoma cells.

The cyclin-dependent kinase inhibitor p21WAF1 participates in cell growth, differentiation, and apoptosis. p21WAF1 can be induced by green tea polyphenol EGCG in several cancer cell types, but its role in the oral cancer cell response to EGCG is not known. We found that EGCG upregulates p21WAF1 in an oral carcinoma cell line, OSC2, by cDNA microarray. The current study determined the impact of siRNA-suppressed p21WAF1 and its response to EGCG on cell growth, DNA synthesis and apoptosis by RT-PCR, Western blot, BrdU incorporation, MTT and caspase 3 activity assays. Suppression of p21WAF1 by siRNA resulted in an accelerated cell growth and DNA synthesis, and increased cell viability. However, caspase 3 activity was not significantly inhibited. The evidence showed that p21WAF1 is involved in EGCG-induced growth arrest of OSC2 cells, which may facilitate caspase 3-mediated apoptosis. Thus, expression of functional p21WAF1 may promote phytochemical-mediated growth arrest and apoptosis in oral carcinoma cells.

Green tea polyphenol-induced epidermal keratinocyte differentiation is associated with coordinated expression of p57/KIP2 and caspase 14.

Epigallocatechin-3-gallate (EGCG), the most abundant polyphenol in green tea, exerts chemopreventive effects by selectively inducing apoptosis in tumor cells. In contrast, EGCG accelerates terminal differentiation in normal human epidermal keratinocytes (NHEK) mediated partially by up-regulation of p57/KIP2, a cyclin-dependent kinase inhibitor that confers growth arrest and differentiation. However, it is unclear if EGCG modulates caspase 14, a unique regulator of epithelial cell terminal differentiation associated with cornification. Here, we examined the effect of EGCG on caspase 14 expression in NHEK and correlated the protein and mRNA expression of p57/KIP2 with those of caspase 14 in either normal keratinocytes or p57/KIP2-expressing tumor cells (OSC2, an oral squamous cell carcinoma cell line). Additionally, paraffin-embedded normal and untreated psoriatic (aberrant keratinization) skin sections from humans were assessed for caspase 14 by immunohistochemistry. In NHEK, EGCG induced the expression of caspase 14 mRNA and protein levels within a 24-h period. The expression of p57/KIP2 in OSC2 cells was adequate to induce caspase 14 in the absence of EGCG; this induction of caspase 14 was down-regulated by transforming growth factor-beta1. In human psoriatic skin samples, caspase 14 staining in the upper epidermis was reduced, especially in nuclear areas. These results suggest that, in addition to p57/KIP2, EGCG-induced terminal differentiation of epidermal keratinocytes involves up-regulation of caspase 14. Further understanding of how EGCG modulates cellular differentiation may be useful in developing green tea preparations for selected clinical applications.

Protective effects of EGCG on salivary gland cells treated with gamma-radiation or cis-platinum(II)diammine dichloride.

Dysfunction of salivary glands is often associated with aging and cancer therapy. Green tea polyphenols were previously found to protect normal epithelial cells from reactive oxygen species, and to induce apoptosis in tumor cells. The current study investigated whether -(-) epigallocatechin-3-gallate (EGCG), the major green tea polyphenol, protects normal salivary gland cells from the effects of gamma-irradiation and the chemotherapy drug cis-platinum(II)diammine dichloride (CDDP). Human immortalized salivary acinar and ductal cells, and oral squamous cell carcinoma cells were irradiated with gamma-rays or treated with CDDP, with or without pretreatment with EGCG, followed by MTT and BrdU incorporation assays. The results demonstrated that EGCG protected the normal salivary gland cells from chemical or irradiation-induced damage. However, protection of oral cancer cells by EGCG was also observed if EGCG was at physiologically achievable salivary concentrations but not at higher concentrations, suggesting that the combination of green tea consumption with cancer therapy requires further evaluation.

Alterations of cell lipids by metal salts.

Metallic medical devices undergo degradation in vivo and the degradation products affect the chemistry and biological responses of cells and tissues in the immediate vicinity. The responses vary with the metal and cell type. In the current study, we examined the effects of several metals on a human monocytic cell line. Monocytes are important effector cells capable of responding rapidly to inflammatory and immune stimuli in a variety of ways, including production of inflammatory proteins, differential expression of surface adhesion molecules, enhanced phagocytic activity, and activation and differentiation to macrophages. Cells were exposed in the presence of (14)C-acetate to titanium, nickel, chromium, copper, or cobalt or vanadium at concentrations that were subinhibitory or inhibitory based on cellular mitochondrial dehydrogenase activity. Cell lipids were then extracted, separated by thin layer chromatography, and quantitated by liquid scintillation spectrometry. Total cell protein also was measured. Titanium reduced cell protein content at concentrations that were noninhibitory to mitochondrial dehydrogenase activity, whereas neither chromium nor cobalt affected protein amounts at dehydrogenase-inhibitory concentrations. In cells exposed to vanadium, the protein- and dehydrogenase-inhibitory concentrations were similar. The major effects on cell lipids appeared to occur in the neutral lipids, although chromium, cobalt, and titanium produced changes in some major phospholipids. These results suggest that metals differentially affect various metabolic pathways in THP-1 cells, perhaps related to their abilities to enter the cells or interact with the membrane. These alterations to the cells may affect the cells' abilities to respond to various stimuli that can damage the tissues.

Induction of apoptosis in oral cancer cells: agents and mechanisms for potential therapy and prevention.

Oral cancer is one of the most disfiguring types of cancer, since the surgical removal of the tumor may result in facial distortion. Oral cancer is also known to exhibit "field cancerization", resulting in the development of a second primary tumor. Furthermore, the five-year survival rate of this disease has remained approximately 50% during the past 30 years. Prevention and early detection/treatment of oral cancer could significantly improve the quality of life for individuals at risk. Recently, the targeted elimination of oral squamous cell carcinoma cells by inducing apoptosis has emerged as a valued strategy to combat oral cancer. Studies utilizing a variety of chemical or biological interventions demonstrated promising results for induction of apoptosis in oral malignant cells. This review summarizes the results of a number of investigations focused specifically on induction of apoptosis in oral cancer cells by synthetic compounds and naturally occurring chemopreventive agents with apoptotic potential.

Roles of catalase and hydrogen peroxide in green tea polyphenol-induced chemopreventive effects.

The green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) possesses promising anticancer potential. Although in vivo studies unveiled the metabolic routes and pharmacokinetics of EGCG and showed no adverse effects, in vitro studies at high concentrations demonstrated oxidative stress. EGCG causes differential oxidative environments in tumor versus normal epithelial cells, but the roles that EGCG, hydrogen peroxide (H2O2), and intracellular catalase play in the epithelial system are largely unknown. The current study employed enzyme activity assays, reactive oxygen species quantification, and immunoblotting to investigate whether EGCG-induced differential effects correlate with levels of key antioxidant enzymes and H2O2. It was found that normal human keratinocytes with high catalase activity are least susceptible to H2O2, whereas H2O2 caused significant cytotoxicity in oral carcinoma cell lines. However, the EGCG-induced differential effects could not be duplicated by H2O2 alone. The addition of exogenous catalase failed to completely prevent the EGCG-induced cytotoxicity and rescue the EGCG-induced growth arrest in the tumor cells. The antioxidant N-acetyl-L-cysteine rescued the tumor cells from H2O2-induced damage only, but not from EGCG-induced mitochondrial damage. Finally, alterations in catalase or superoxide dismutase activities were not observed upon EGCG exposure. In conclusion, although endogenous catalase may play a role in response to H2O2-induced cytotoxicity, the EGCG-induced cytotoxic effects on tumor cells mainly result from sources other than H2O2.

Green tea polyphenol causes differential oxidative environments in tumor versus normal epithelial cells.

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, (-)-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.

Vascular responsiveness to dimethylaminoethyl methacrylate and its degradation products.

The increasing use of acrylate-based resins in dentistry has raised questions about the biocompatibility of these substances with oral tissues. The focus of the present investigation was to assess the responsiveness of blood vessels to the resin polymerization accelerating agent dimethylaminoethyl methacrylate (DMAEMA) and its degradation products dimethylethanolamine (DME) and methacrylic acid (MAA), using the rat aortic ring preparation as a tissue model. DMAEMA induced concentration-dependent relaxation of norepinephrine (NE)-contracted aortic rings with and without endothelium. N-nitro-L-arginine methyl ester (L-NAME) selectively inhibited the endothelium-dependent relaxation induced by DMAEMA, suggesting the release of nitric oxide from the endothelium by DMAEMA. Both indomethacin and glybenclamide attenuated the vasorelaxation elicited by DMAEMA in the presence as well as in the absence of endothelium, providing evidence for the role of vasorelaxant prostanoid(s) and K(ATP) channel activation in the responses observed. On the other hand, while MAA was without any apparent effect on the rat aorta, DMAEMA at high and DME at relatively low concentrations caused contraction of the tissues with and without endothelium in the absence of NE. The DME-induced contraction was inhibited by indomethacin, suggesting the involvement of contractile arachidonic acid metabolite(s) in the action of DME. This observation was supported by the findings of increased thromboxane A(2) (TXA(2)) production in aortic rings incubated with DME. Taken together, the data suggest that both DMAEMA and its degradation product, DME, are vasoactive, inducing vasorelaxation and contraction by various mechanisms that may involve the release of nitric oxide from the endothelium, the activation of smooth muscle K(ATP) channels, and the generation of vasorelaxant prostanoid(s) and TXA(2). These effects may play a role in tissue homeostasis and certain adverse conditions associated with the use of dental resin materials containing DMAEMA and/or DME.