The aim of this study was to evaluate the biomechanical behavior and long-term safety of high performance polymer PEKK as an intraradicular dental post-core material through comparative finite element analysis (FEA) with other conventional post-core materials. A 3D FEA model of a maxillary central incisor was constructed. A cyclic loading force of 50 N was applied at an angle of 45° to the longitudinal axis of the tooth at the palatal surface of the crown. For comparison with traditionally used post-core materials, three materials (gold, fiberglass, and PEKK) were simulated to determine their post-core properties. PEKK, with a lower elastic modulus than root dentin, showed comparably high failure resistance and a more favorable stress distribution than conventional post-core material. However, the PEKK post-core system showed a higher probability of debonding and crown failure under long-term cyclic loading than the metal or fiberglass post-core systems.

Oxidative stress is known to induce cell death in a wide variety of cell types, apparently by modulating intracellular signaling pathways. Activation of extracellular signal-regulated kinase (ERK) in oxidative stress remains controversial. In some cellular systems, the ERK activation is associated with protection against oxidative stress, while in other system, the ERK activation is involved in apoptotic cell death. The present study was undertaken to examine the role of ERK activation in H2O2-induced cell death of human glioma (A172) cells. H2O2 resulted in a time- and dose-dependent cell death, which was largely attributed to apoptosis. H2O2 treatment caused marked sustained activation of ERK. The ERK activation and cell death induced by H2O2 was prevented by catalase, the hydrogen peroxide scavenger, and U0126, an inhibitor of ERK upstream kinase MEK1/2. Transient transfection with constitutive active MEK1, an upstream activator of ERK1/2, increased H2O2-induced cell death, whereas transfection with dominant-negative mutants of MEK1 decreased the cell death. The ERK activation and cell death caused by H2O2 was inhibited by antioxidants (N-acetylcysteine and trolox), Ras inhibitor, and suramin. H2O2 produced depolarization of mitochondrial membrane potential and its effect was prevented by catalase and U0126. Taken together, these findings suggest that growth factor receptor/Ras/MEK/ERK signaling pathway plays an active role in mediating H2O2-induced apoptosis of human glioma cells and functions upstream of mitochondria-dependent pathway to initiate the apoptotic signal.

No abstract

Effect of melatonin on toxicity of cadmium (Cd) was studied in male SD rats co-administered daily Cd (1 mg/kg b.w., s.c.) with melatonin (10 mg/kg b.w., i.p.) for 15 days. Cd alone injection decreased GSH concentrations in the liver and RBC by 35% and 43% compared with those in saline-treatment group, but not in the kidney and whole brain. The activity of GSSG-reductase was significantly decreased in the liver of Cd alone injected rats, while melatonin given in combination with Cd failed to prevent the Cd-induced decreased activity of hepatic GSSG-reductase. However, the hepatic GSH concentration decreased by Cd alone was restored by melatonin treatment, and the melatonin also ameliorated Cd-induced histopathological changes in the liver. Therefore, data indicate that melatonin restores the reduction of hepatic GSH level induced with Cd regardless of GSSG-reductase activity, and suggests that melatonin may ameliorate Cd-induced hepatotoxicity.

No abstract