PubMed · 13677850
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W P Maher. 2003. Disagrees with article.. https://pubmed.ncbi.nlm.nih.gov/13677850/
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Bisphenol A (BPA) recognition materials were synthesized by a covalent imprinting technique using BPA-dimethacrylate or BPA-diacrylate as the template monomer. Binding sites in the polymers consisted of two hydroxyl groups that are generated by reducing the ester bonds of the template monomer with lithium aluminum hydride. The polymers strongly adsorbed BPA and structurally related compounds, however, other endocrine disruptors were hardly adsorbed. The BPA-dimethacrylate-based polymer interacted with the samples more strongly than the BPA-diacrylate-based polymer.
This article investigates the transmittance of a new ceramic filling material as a function of time, thickness, wavelength, and addition of pigments. In the hardened state the ceramic material is composed of hydrates, calcium aluminate, and glass fillers. The radiopacity of the investigated material is also measured. The results of the transmittance are compared to a commercial glass ionomer cement (Fuji II) and resin composite (Tetric Ceram). The transmittance increased with time from low values after 1 h to values close to the glass ionomer cements after 1 week. The resin composite had almost twice the transmittance as the calcium aluminate material and the glass ionomer cement. The amount of light passing through the material was dependent on both the sample thickness and the wavelength. Samples of 0.5-mm thickness transmitted almost twice as much as 1-mm-thick samples. Regarding the wavelength, blue light was scattered very effectively (low transmittance), whereas red light was not (high transmittance). Addition of pigments lowered the transmittance. The radiopacity was slightly higher than that of enamel.
Past studies in our laboratory have shown that silica (-quartz) particle exposure of a mouse alveolar macrophage cell line (MH-S) elicits mitochondrial depolarization and caspase 3 and 9 activation, contributing to apoptosis. However, cellular pathways leading to these outcomes have not been extensively investigated. Initial studies revealed that silica exposure elicits lysosomal permeability after 1 h, as evidenced by leakage of FITC-conjugated dextran and acridine orange. We next evaluated a role for the lysosomal acidic compartment in apoptosis. Cells pretreated with the lysosomotropic weak base ammonium chloride, to increase lysosomal pH, showed decreased caspase activation and apoptotic DNA fragmentation. MH-S cells pretreated with pepstatin A, an inhibitor of lysosomal cathepsin D, showed decreased caspase 9 and 3 activation as well as a decreased percentage of cells that became apoptotic. DNA fragmentation and caspase 9 and 3 activation were also decreased in cells pretreated with despiramine, an inhibitor of lysosomal acidic sphingomyelinase. Silica pretreated with aluminum lactate (to blunt surface active sites) reduced caspase activation and apoptosis. Although aluminum lactate-treated silica still induced lysosomal permeability (by FITC-dextran leakage), one measure of lysosome integrity and function suggested a reduction in the extent and/or nature of lysosomal injury (by acridine orange retention). A role for reactive oxygen species (ROS) was investigated to explore another pathway for silica-induced apoptosis in addition to lysosomal enzymes; however, no role for ROS was apparent. Thus, following silica exposure, lysosomal injury precedes apoptosis, and the apoptotic signaling pathway includes cathepsin D and acidic sphingomyelinase.