Identifying enzyme activities within human saliva which are relevant to dental resin composite biodegradation.

Esterase activities similar to those of cholesterol and pseudocholine esterases (CE and PCE, respectively) have been detected within whole human saliva. Since commercial CE has been shown to possess distinct activity relative to PCE for select components in dental composites, it is hypothesized that esterases isolated from human saliva will also show selectivity towards specific monomer elements within the composites. The objective of this work was to carry out the isolation of these activities from whole human saliva and study their individual effects on resin monomers such as Bis-phenyl glycidyl dimethacrylate (aromatic structure) and triethylene glycol dimethacrylate (hydrophilic structure), and on cured composites containing the latter monomers. Human saliva samples were processed, fractionated on a gel filtration column and assayed for CE and PCE-like activity. Selected fractions were incubated at 37 degrees C with the above monomers and select commercial composites. Degradation was monitored using high-performance liquid chromatography. The fraction with the highest cholesterol esterase-like character preferentially degraded the aromatic monomer and significantly degraded more of the composite's material relative to a fraction containing low amounts of the cholesterol esterase activity but elevated pseudocholine esterase-like activity. Hence, it was concluded that select salivary esterases had preferences for distinct composite resin components.

The removal of extracellular calcium: a novel mechanism underlying the recruitment of N-methyl-D-aspartate (NMDA) receptors in neurotoxicity.

The involvement of NMDA-type glutamate receptor in neuronal injury established in experimental stroke and neurotrauma models has been recently challenged by failures in treatment of stroke/neurotrauma patients with NMDA receptor antagonists. NMDA receptor activity is known to be essential for mediating a multitude of physiological functions. However, how NMDA receptors are recruited to cause neuronal injury remains unclear. Here we report that the time period during which initial NMDA receptor up-regulation occurs is critical for the recruitment of NMDA receptors causing neuronal injury during extracellular calcium (Ca2+) reperfusion in cultured hippocampal neurons, and represents the key period for neuronal protection by NMDA receptor antagonists. Furthermore, we identified that via intracellular sodium (Na+), extracellular Ca2+ depletion induces the up-regulation of NMDA receptor gating. Taken together, our study provides direct experimental evidence suggesting that determination of when and how NMDA receptors are recruited to cause neurotoxicity is essential for guiding treatment via antagonism of NMDA receptor functions.