The reaction of singlet oxygen (1O2) generated by ultraviolet-A (UVA)-visible light (lambda > 330 nm) irradiation of air-saturated solutions of hematoporphyrin with phenolic compounds in the presence of a spin trap, 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), gave an electron spin resonance (ESR) spectrum characteristic of the DMPO-hydroxyl radical spin adduct (DMPO-*OH). In contrast, the ESR signal of 5,5-dimethyl-2-pyrrolidone-N-oxyl, an oxidative product of DMPO, was observed in the absence of phenolic compounds. The ESR signal of DMPO-*OH decreased in the presence of either a *OH scavenger or a quencher of *O2 and under anaerobic conditions, whereas it increased depending on the concentration of DMPO. These results indicate both 1O2- and DMPO-mediated formation of free *OH during the reaction. When DMPO was replaced with 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline-N-oxide (DEPMPO), no DEPMPO adduct of oxygen radical species was obtained. This suggests that 1O2, as an oxidizing agent, reacts little with DEPMPO, in which a strong electron-withdrawing phosphoryl group increases the oxidation potential of DEPMPO compared with DMPO. A linear correlation between the amounts of DMPO-*OH generated and the oxidation potentials of phenolic compounds was observed, suggesting that the electron-donating properties of phenolic compounds contribute to the appearance of *OH. These observations indicate that 1O2 reacts first with DMPO, and the resulting DMPO-1O2 intermediate is immediately decomposed/reduced to give *OH. Phenolic compounds would participate in this reaction as electron donors but would not contribute to the direct conversion of 1O2 to *OH. Furthermore, DEPMPO did not cause the spin-trapping agent-mediated generation of *OH like DMPO did.

Guaiacol, which is a phenolic compound with a methoxy group and used in traditional dental pulp sedation, has the property of inducing cell proliferation. To clarify these mechanisms of guaiacol, this study examined the hydroxyl radical (• OH) scavenging effects of guaiacol in vitro. Generation of• OH was carried out by the Fenton reaction using mixture of ascorbic acid, H 2 O 2 , and Fe(III)-EDTA, and• OH was detected by measuring the • OH-mediated production of degradation products of deoxyribose, which reacts with 2-thiobarbituric acid (TBA) and is relatively stable for a long time. At concentrations of 10 −10 M to 10 −3 M, guaiacol inhibited the TBA reactive substance (TBA-RS) formation in a dose-dependent manner. Phenol and formaldehyde were also found to inhibit the TBA-RS formation, but their inhibitory activities were lower than that of guaiacol. The concentrations of guaiacol, phenol, and formaldehyde needed to cause 50% inhibition of TBA-RS formation were approximately 5 × 10 , and 2 × 10 −3 M, respectively. In this reaction system, guaiacol showed no chelating reaction with ferrous ion and did not directly react with H 2 O 2 . Guaiacol also exhibited radical scavenging activity on 1,1-diphenyl-2-picrylhydrazyl (DPPH) stable free radical, but its scavenging activity was lower than that toward•

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The effects of various anticonvulsants on local anaesthetics procaine- and lidocaine-induced convulsions were investigated in rats. Pretreatment with diazepam (2.5-5 mg/kg, intraperitoneally) and clonazepam (5-10 mg/kg, intraperitoneally) completely protected the rats against both local anaesthetic-induced convulsions. Phenobarbital (12.5-50 mg/kg, subcutaneously) also significantly decreased the incidence of both convulsions and prolonged their latencies. Carbabazepine (10-40 mg/kg, intraperitoneally) did not completely repress both convulsions, but it prolonged their latencies. Phenytoin (5-20 mg/kg, intraperitoneally) and primidone (30-60 mg/kg, intraperitoneally) markedly enhanced both local anaesthetic-induced convulsions, as shown by shortening of latency and increase in mortality. Valproate (100-200 mg/kg, intraperitoneally) produced a protective effect against procaine-induced convulsions, while it strongly enhanced lidocaine-induced convulsions. These results suggest that the benzodiazepines are effective drugs to prevent neurotoxicity induced by local anaesthetics, while phenytoin and primidone potentiate them.

The purpose of this study was to evaluate the tensile bond strength to peroxide-exposed dentin. Furthermore, the effect of ascorbic acid on the bond strength of peroxide-exposed dentin was investigated. Extracted bovine dentin was exposed to 10% carbamide peroxide, 30% hydrogen peroxide or distilled water for 30 min, then treated with 10% ascorbic acid (0,30, 90, 180 min), and conditioned with 10% citric acid/3% ferric chloride. The PMMA rod was bonded to the treated bovine dentin with 4-META/MMA-TBB resin. A mini-dumbbell-shaped bonded specimen was prepared from these bonded assemblies and the tensile bond strength was tested. The fractured surfaces were also observed with SEM. Exposure to peroxide before bonding significantly reduced bond strength. The application of ascorbic acid to the peroxide-exposed dentin increased bond strength. On the other hand, an adverse effect of ascorbic acid was found in distilled water-affected dentin.Extended resin fibers were partially seen in the peroxide-exposed dentin. In conclusion, peroxide reduced the bond strength, and the stronger the oxidation, the weaker the obtained bond. Anti-oxidation with ascorbic acid recovered the bond strength, and the effect increased the longer the ascorbic acid was applied.