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PubMed2006

Identification and estrogenic characterization of impurities in commercial bisphenol A diglycidyl ether (BADGE).

A sample of commercial BADGE was fractioned by HPLC and eight impurities including novel propyl derivatives (2), (5) and (6) were identified by NMR spectrometry, FAB-MS and GC-MS. The estrogenicity, both agonist and antagonist, of fractions containing these impurities was measured with a yeast two-hybrid assay incorporating the human (hER alpha) and a competitive binding assay for hER alpha (ELISA). In the yeast two-hybrid assay, estrogenic antagonist activity was found in two fractions, while estrogenic agonist activity was not found in any. In the ELISA method, the binding affinity to hER alpha was found in three fractions. It is probable that a comprehensive assessment of the estrogenic properties of commercial BADGE, and their implications for human health, will require examination of all its components as described here.

Animals↗
PubMed2004

Steroid activities comparison of natural and food wrap compounds in human breast cancer cell lines.

In this study, we tested and compared the endocrine disruption activities of compounds in materials used to package foods (bisphenol A, bisphenol F, and bisphenol A diglycidylether BADGE) with natural molecules (genistein, apigenin, kaempferol, and tangeretin) in the human breast cancer cell lines MCF-7 (ER(+)) and MDA-MB453 (AR(+); GR(+)). Octylphenol was also chosen as a xenoestrogen reference. Two compounds had no estrogenic activity: BADGE and tangeretin. Genistein was the most active compound in the E-Screen assay with MCF-7, followed by octylphenol, bisphenol F, bisphenol A and apigenin, with kaempferol the least potent. All estrogenic compounds competed with 17beta-estradiol for binding to the MCF-7 ER and their estrogenic effects were abolished in the presence of tamoxifen, an ER antagonist. In MDA-MB453 cells transfected with pMMTVneo-Luc, all compounds had anti-androgenic activities, with octylphenol the most potent. Kaempferol, genistein, and apigenin were more potent anti-androgens than bisphenols A or F. The natural compounds had a biphasic effect on luciferase activity. At high concentrations, genistein (10(-5)M) and apigenin (10(-6)M) acted as GR agonists in transfected MDA-MB453 cells. Furthermore, apigenin, at a concentration of 10(-5)M, may act as a partial androgen receptor (AR) agonist, as nilutamide, an AR antagonist, inhibited its activity by 26%.

Anticarcinogenic Agents↗
PubMed2000

Microtensile bond strengths of seven dentin adhesive systems.

OBJECTIVES: The purpose of this study was to evaluate the microtensile bond strengths of seven dentin adhesive systems (Solid Bond, EBS-Multi, PermaQuik, One Coat Bond, Gluma One Bond, Prime & Bond NT/NRC and Clearfil Liner Bond 2V) and their respective fracture modes. METHODS: Superficial occlusal dentin of extracted human molars was exposed, finished with wet 600-grit silicon carbide paper, and a block of resin composite bonded with the above adhesives according to the manufacturers' instructions. The teeth were kept in tap water for 24 h at 37 degrees C, sectioned to obtain three or four bar-shaped specimens, which were then shaped to an hour-glass form of 1.2 +/- 0.02 mm diameter. The specimens were stressed at a crosshead speed of 1 mm/min until rupture of the bond. The mean bond strengths were compared using one-way ANOVA and LSD tests. The frequency of fracture modes was compared using Kruskal-Wallis and Mann-Whitney U-tests. RESULTS: Mean microtensile bond strengths ranged from (17.8 +/- 7.0) MPa for Solid Bond to (36.0 +/- 8.1) MPa for Clearfil Liner Bond 2V. The bond strength of Clearfil Liner Bond 2V and PermaQuik (30.8 +/- 8.5 MPa) were not significantly different, and were higher than all other materials. Bond strengths of Solid Bond (17.8 +/- 7.0) MPa, EBS-Multi (18.7 +/- 5.0) MPa, One Coat Bond (21.9 +/- 5.6) MPa, and Gluma One Bond (23.4 +/- 5.2) MPa were not significantly different. SEM examination indicated that Solid Bond, EBS-Multi and One Coat Bond showed no significant difference in failure modes but were significantly different from PermaQuik, Prime & Bond NT/NRC and Clearfil Liner Bond 2V. SIGNIFICANCE: The self-etching primer system, Clearfil Liner Bond 2V, provided the simplest bonding technique, and together with PermaQuik exhibited greatest bond strength to dentin.

Analysis of Variance↗
PubMed2004

Kinetic isotope effects implicate the iron-oxene as the sole oxidant in P450-catalyzed N-dealkylation.

Multiple oxidants have been implicated as playing a role in cytochrome P450-mediated oxidations. Herein, we report results on N-dealkylation, one of the most facile reactions mediated by P450 enzymes. We have employed the N-oxides of a series of para-substituted 13C2H2-labeled N,N-dimethylanilines to function as both substrates and surrogate oxygen atom donors for P450cam and P4502E1. Kinetic isotope effect profiles obtained using the N-oxide system were found to closely match the profiles produced using the complete NAD(P)H/NAD(P)-P450 reductase/O2 system. The results are consistent with oxidation occurring solely through an iron-oxene species.

Alkylation↗
PubMed2005

Design and synthesis of a DNA-crosslinking azinomycin analogue.

The azinomycins are potent antitumour antibiotics that are able to crosslink DNA, but are relatively unstable and unlikely to progress as therapeutic candidates. A prototype analogue 4 with more clinical potential has been designed and synthesised and incorporates the epoxide function of the azinomycins and a nitrogen mustard. Two further analogues 5 and 6 that can alkylate DNA but cannot crosslink the duplex have also been synthesised. Compound 4 crosslinks DNA efficiently at nM concentrations. Compounds 4-6 were submitted to the NCI 60 cell line screen and have similar antitumour activity, although 4 is slightly less active than the non-crosslinking compounds. These observations will be important in the design of further azinomycin analogues with antitumour activity.

Alkylation↗
PubMedDate not supplied

Health and economic consequences of sevelamer use for hyperphosphatemia in patients on hemodialysis.

OBJECTIVES: The safety and efficacy of sevelamer hydrochloride in binding phosphate in patients with end-stage renal disease and its ability to attenuate the progression of cardiac calcification have been well documented but not the longer-term health and economic implications. Thus, a model of the predicted long-term consequences of sevelamer compared with calcium-based binders (acetate and carbonate) was developed. METHODS: Long-term cardiovascular implications of 1 year of treatment with phosphate binders in patients on hemodialysis are estimated based on the patient's demographics, comorbidities, and physiologic and renal parameters. The initial calcification score and expected changes over 1 year are derived using regression equations developed from the Treat-to-Goal study and translated to cardiovascular disease risk based on equations developed from a long-term cohort study. In this article, the implications of cardiovascular disease for life expectancy and medical costs are accounted for from a US payer perspective. RESULTS: The cardioprotective effect of sevelamer over 1 year is estimated to result in a 12% reduction in cardiovascular events compared with calcium acetate. In a population of 100 patients, the savings of 205,600 dollars accrued due to avoiding nine cardiovascular events with sevelamer, largely offset the increased binder costs, leading to a favorable cost-effectiveness ratio of about 2200 dollars per (discounted) life-year gained. CONCLUSIONS: Although both binders provide equivalent phosphate binding capacity, the results indicate that the advantage of 1 year of treatment with sevelamer in attenuating the progression of calcification has important clinical and economic consequences, suggesting that this provides good value for money.

Acetates↗
PubMed1999

Characterization of the reactivity, regioselectivity, and stereoselectivity of the reactions of butadiene monoxide with valinamide and the N-terminal valine of mouse and rat hemoglobin.

Occupational exposure to 1,3-butadiene (BD) has been monitored by measuring the level of hemoglobin N-terminal valine adduct formation with the primary reactive metabolite, butadiene monoxide (BMO). However, mechanistic details concerning the relative reactivity, regioselectivity, and stereospecificity of BMO with the N-terminal valine of hemoglobin are lacking. In the studies presented here, L-valinamide was used as a model for the N-terminal valine of hemoglobin to compare the nucleophilic reactivity, regioselectivity, and stereoselectivity of the reaction both in aqueous solution and within a protein microenvironment. Four products produced by the reaction of L-valinamide with racemic BMO (two pairs of diastereomers produced by reactions at C-1 and C-2 of the epoxide moiety) were synthesized, purified, and characterized by (1)H NMR and GC/MS. These four reaction products were used as analytical standards for kinetic studies of the reaction of valinamide with BMO at physiological pH (7.4) and temperature (37 degrees C). The results show that the adducts formed by reaction at C-2 were formed at a ratio of approximately 2:1 compared to the adducts formed by reaction at C-1. The stereoisomers of each respective regioisomer were produced with similar rates of formation. The reaction of BMO with the N-terminal valine of hemoglobin was also studied in vitro using intact erythrocytes from Sprague-Dawley rats and B6C3F1 mice. After cleavage of the N-modified valine by the N-alkyl Edman degradation procedure using pentafluorophenylisothiocyanate (PFPITC), a novel procedure was developed that allowed GC/MS detection and quantitation of the four expected products by silylation of the PFPTH-valine-BMO derivatives. The hemoglobin results contrast with the valinamide results in that the reaction of BMO with the N-terminal valine residue in both rat and mouse hemoglobin produced mostly C-1 adducts. The rates obtained with rat hemoglobin were much slower than the rates obtained with mouse hemoglobin or with valinamide. These results, and the finding that the reaction with rat hemoglobin produced a higher ratio of C1:C2 adducts in comparison with the reaction with mouse hemoglobin, indicate the importance of measuring all four adducts when comparing the relative rates of adduct formation both with model compounds and among different species.

Animals↗
PubMed1984

Antileukemic compounds derived by chemical modification of macrocyclic trichothecenes. 2. Derivatives of roridins A and H and verrucarins A and J.

Various 8 beta-hydroxy, 16-hydroxy, and 9 beta,10 beta-epoxy derivatives of roridins A and H and verrucarins A and J have been prepared and tested in vivo against P388 mouse leukemia. The 9 beta,10 beta-epoxy derivatives and 16-hydroxy derivatives consistently exhibit very high activity. The 8 beta-hydroxy-9 beta,10 beta-epoxy and 16-hydroxy-9 beta,10 beta-epoxy derivatives of verrucarin A and roridin A exhibit extraordinary activity against P388. The 8 beta-hydroxy-9 beta,10 beta-epoxy and 16-hydroxy-9 beta,10 beta-epoxy derivatives of verrucarin A and roridin A exhibit extraordinary against P388.

Animals↗
PubMed1977

Metabolic activation of diethylstilbestrol and aminostilbene-derivatives.

Diethylstilbestrol and trans-4-dimethylaminostilbene are metabolically activated and several of their metabolites are able to react with cellular macromolecules. Some of the problems are discussed which are encountered in linking a particular metabolite with the mutagenic and carcinogenic properties of these compounds.

Animals↗
PubMed1999

Bisphenol-A content of resin monomers and related degradation products.

Recently, it was reported that Bisphenol-A (BPA) was released from one fissure sealant (Delton) into saliva causing estrogenic activity in vitro. The aim of this study was to chemically analyze the BPA content of different fissure sealant resin monomers and their release of BPA under hydrolytic conditions. BPA content was first measured in commercially available monomers of bisphenol-A glycidyldimethacrylate (Bis-GMA), bisphenol-A dimethacrylate (Bis-DMA) and bisphenol-A diglycidylether (BADGE). Then, Bis-GMA-monomer and Bis-DMA-monomer in methanol were subjected to pH values of 0 to 11 for 30 minutes at 50 degrees C, to porcine liver esterase, and to pooled saliva for up to 24 hours. The BPA-content was determined by high-performance liquid chromatography (HPLC). Bis-GMA-monomer and BADGE-monomer from one manufacturer did not contain any detectable amounts of BPA (< or = 2 ppm); Bis-DMA and BADGE-monomer from a second manufacturer contained BPA quantities of 4-155 ppm. For Bis-GMA-monomer, no BPA could be detected under any hydrolytic conditions chosen (detection limit: < or = 1%). For Bis-DMA-monomer an increase of BPA was observed at pH 11, resulting in a conversion of approx. 100% Bis-DMA to BPA. When Bis-DMA was subjected to esterase, a conversion of 82.5% resulted after 24 h; saliva led to an 81.4% conversion of Bis-DMA after 24 h. Hence, we conclude that the results reported in the literature may be attributed to the Bis-DMA-content of the fissure sealant tested (Delton). No BPA-release is expected under physiologic conditions from fissure sealants based on Bis-GMA if pure base monomers are used.

Benzhydryl Compounds↗
PubMed1999

Calcified plaque cross-sectional area in human arteries: correlation between intravascular ultrasound and undecalcified histology.

BACKGROUND: The purpose of this investigation was to quantify the amount of intralesional calcium detected by intravascular ultrasound (IVUS) compared with undecalcified histology in human arteries. This method preserves intralesional calcium and reduces sectioning artifacts, thereby providing an accurate measure of calcium plaque morphology. METHODS AND RESULTS: Ten arterial segments (5 coronary, 5 iliac) were obtained at autopsy. IVUS imaging was performed with a 4.9F catheter at an automated pullback rate of 1.0 mm/s. The undecalcified arteries were dehydrated in ascending alcohol and polymerized in glycol methylmethacrylate. The arteries were cut into 200-microm sections with an Isomet low-speed saw and stained with Goldner's trichrome. The lumen cross-sectional area, the calcium plaque cross-sectional area, the calcium plaque depth, length, and angle of arc of calcified plaque were measured from the IVUS images and histologic sections. In 24 selected cross sections, there were 38 separate calcium plaques. An independent observer correctly identified 34 of 38 calcified plaques for a sensitivity of 89% and specificity of 97%. The total mean calcified plaque cross-sectional area measured from histology was 4.6 +/- 4.1 mm2 compared with 2.8 +/- 2.3 mm2 by IVUS (P =.002). Plaque depth measured by histology was 1.2 +/- 0.4 mm versus 0.7 +/- 0.2 mm by IVUS (P =.001). The length of calcium plaques measured by histology was 3.6 +/- 1.78 mm versus 3.6 +/- 1.5 mm for IVUS (r = 0.79). CONCLUSIONS: IVUS accurately depicts circumferential calcified lesions with high sensitivity (89%) and specificity (97%). However, IVUS underestimates the total calcified plaque cross-sectional area by 39%. This is mainly because of the inability of the ultrasound to penetrate intralesional calcium, which leads to an underestimation of the depth of calcium by 45%.

Adult↗
PubMed2002

Antidiabetic thiazolidinediones inhibit collagen synthesis and hepatic stellate cell activation in vivo and in vitro.

BACKGROUND & AIMS: The ligand-dependent transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) is expressed in hepatic stellate cells (HSC), and its transcriptional activity is reduced during cell transdifferentiation in culture. PPARgamma transcriptional activation decreases platelet-derived growth factor-induced proliferation and inhibits alpha-smooth muscle actin expression in cultured HSC. The aim of our study was to evaluate whether oral administration of synthetic PPARgamma ligands, thiazolidinediones (TZD), might affect collagen deposition in animal models of liver fibrosis. METHODS: The effect of 2 TZD (pioglitazone or rosiglitazone) was tested on liver fibrosis induced in rats by either toxin administration (dimethylnitrosamine or carbon tetrachloride) or bile duct ligation. In vivo PPARgamma activation was evaluated by gel shift assay using nuclear extracts from HSC isolated from control and treated rats. RESULTS: Oral administration of TZD reduced extracellular matrix deposition and HSC activation in both toxic and cholestatic models of liver fibrosis. PPARgamma-specific DNA binding was significantly impaired in nuclear extracts of HSC isolated from fibrotic rats compared with HSC from control rats. TZD administration restored PPARgamma DNA binding in HSC nuclei. In vitro, TZD-induced PPARgamma activation inhibited collagen and fibronectin synthesis induced by transforming growth factor (TGF)-beta1 in human HSC, as measured by enzyme-linked immunosorbent assay and Northen blotting. TZD also reduced the TGF-beta1-induced activity of a 3.5-kilobase procollagen type I promoter transfected in human HSC. CONCLUSIONS: These findings indicate that PPARgamma activation in HSC retards fibrosis in vivo and suggest the use of TZD for the treatment of liver fibrosis.

Animals↗
PubMed1998

2,3-epoxy-4-hydroxynonanal, a potential lipid peroxidation product for etheno adduct formation, is not a substrate of human epoxide hydrolase.

Our previous studies have shown that 2,3-epoxy-4-hydroxynonanal, a reactive epoxy aldehyde capable of forming etheno adducts with DNA bases, is mutagenic and tumorigenic (Carcinogenesis, 14, 2073). The epoxy aldehyde can be generated from trans-4-hydroxy-2-nonenal, a lipid peroxidation product of omega-6 polyunsaturated fatty acids, by autoxidation or by incubation with fatty acid hydroperoxides or hydrogen peroxides (Chem. Res. Toxicol., 9, 306). These are plausible in vivo pathways for the formation of 2,3-epoxy-4-hydroxynonanal. The possibility that 2,3-epoxy-4-hydroxynonanal is a tumorigen of endogenous origin is suggested by recent observations that etheno bases are detected as background DNA lesions in untreated rodents and humans. A metabolic pathway critical for detoxification of 2,3-epoxy-4-hydroxynonanal involves the ring-opening by epoxide hydrolase, which abolishes its ability to form cyclic etheno DNA adducts. In this study, we examined whether 2,3-epoxy-4-hydroxynonanal is a substrate of cDNA expressed human epoxide hydrolase. Human epoxide hydrolase was expressed in TK- 143 cells (thymidine kinase-deficient human embryoblast) infected with recombinant vaccinia virus encoding human epoxide hydrolase cDNA. Controls consisted of the cells infected with vaccinia virus in the absence of human epoxide hydrolase cDNA. No hydrolysis occurred when [2,3-(3)H]2,3-epoxy-4-hydroxynonanal was incubated at 37 degrees C for 30 min at pH 7.4 with cells expressing human epoxide hydrolase, as indicated by the presence of a pair of radioactive peaks in reversed-phase HPLC chromatography, which comigrated with the UV standards of the two diastereomers of the epoxy aldehyde. The identity of these compounds as the intact epoxy aldehyde was further supported by derivatization to the 2,4-dinitrophenylhydrazones followed by reversed phase HPLC analysis. Similar results were observed with the control cells or with the heat deactivated human epoxide hydrolase. The epoxide hydrolase activity in the expressed cells was demonstrated by their ability to convert benzo[a]pyrene-4,5-dihydroepoxide to benzo[a]pyrene-trans-4,5-dihydrodiol under the same conditions. These results clearly indicate that 2,3-epoxy-4-hydroxynonanal is not a substrate of human epoxide hydrolase, and, thus strengthen its possible endogenous role in the formation of promutagenic exocyclic etheno adducts in vivo.

Aldehydes↗