To examine if human dental pulp cells are useful for assessing the carcinogenic potential of chemical agents, we cultured human dental pulp cells from adults and studied the ability of chemical agents known to be carcinogenic to induce chromosome aberrations in these cells. We confirmed that human dental pulp cells in primary or secondary cultures had the capability of accumulating calcium in vitro as detected by Alizarin red staining and generating dentin-like tissue in immunocompromised mice. These phenotypes were maintained even in cells at seven passages. Next, we examined if chromosome aberrations were induced by exposure of human dental pulp cells (designated here as D824 cells) at seven to nine passages to chemical agents with carcinogenic activity. Statistically significant increases in the frequencies of chromosome aberrations were induced in D824 cells treated with a direct-acting carcinogen, mitomycin C, for 3 h. Chromosome aberrations were also induced at statistically significant levels in D824 cells treated with an indirect-acting carcinogen, cyclophosphamide, for 2 h in the presence of exogenous metabolic activation with rat liver postmitochondrial supernatant. Cyclophosphamide failed to induce chromosome aberrations in the absence of exogenous metabolic activation. Although the reliability of chromosome aberration tests using human dental pulp cells remains to be validated by studying the ability of various other chemical agents with or without carcinogenic activity to induce chromosome aberrations, this chromosome aberration test system may be useful for carcinogenic risk assessment in the target cells.
To determine the adverse effects against human dental pulp tissue, the sensitivity of human dental pulp cells (D824 cells) to 18 chemical agents used for endodontic treatments in dentistry was examined. The cytotoxicity, as determined by a decrease in colony-forming ability of cells treated with the chemical agents, increased as the concentration increased. As a quantitative measure of the cytotoxic effect, LC(50), the concentration which induces a 50% lethality, was extrapolated from the concentration-response curves. The rank of the chemical agents according to their cytotoxic effect (LC(50)) was sodium arsenite > formaldehyde > hydrogen peroxide > zinc oxide > thymol ≈ iodoform ≈ eugenol > guaiacol > ethylenediaminetetraacetic acid ≈ iodine > procaine > lidocaine ≈ chloramphenicol ≈ m-cresol > calcium hydroxide ≈ sodium hypochlorite ≈ phenol ≈ p-phenolsulfonic acid. To compare the cytotoxicity and the levels of apoptosis and mRNA expression of five genes related to the function of dental pulp tissue, D824 cells treated with the LC(50) concentrations of chemical agents were assayed by the TUNEL method and quantitative reverse transcription polymerase chain reaction analysis, respectively. The inducibility of apoptotic cells and the level of mRNA expression of the genes varied with the chemical agents, indicating that both effects occurred independent of the rank of cytotoxic effect of the chemical agents. The results not only provide information concerning cytotoxicity of various chemical agents to human dental pulp cells, but also show an insight into the diversity of the pharmacodynamic action of the chemical agents.
Angioleiomyoma in the buccal space is a less common benign neoplasm. To the best of our knowledge, only two cases have been described. We herein describe a new case of angioleiomyoma in the buccal space of a 45-year-old Japanese woman. No specific features were observed on clinical examination or ultrasonography. With an initial diagnosis of an ectopic lymph node or benign tumor, excision via the oral cavity was performed under local anesthesia. Healing was uneventful. Immunohistochemical examination revealed that the excised specimen was progesterone receptor-positive and estrogen receptor-negative.
ABSTRACT. To elucidate the pathogenesis of halothane-induced hepatopathy, the changes of hepatic tissue phospholipid peroxidation, malondialdehydes (MDAs), and antioxidative enzyme activities were examined in the portal vein arterialized dogs with halothane inhalation. In group A, which was given halothane inhalation under the hepatic blood flow volume less than 10% of pre-operation volume designated as a hypoxic condition, peroxidized phosphatidylcholine (PC), and free and protein-bound MDA levels significantly increased after inhalation. Although the level of protein bound MDA in group C, given hypoxic condition alone, also increased during the experimental period, the response of this was smaller than that in group A, suggesting that the halothane inhaltation enhanced free radical generation under the hypoxic condition. In contrast, no significant changes of these levels were observed in groups B and D, both of which were supplied with sufficient hepatic oxygen as the normoxic condition. In addition, the significant negative correlations between hepatic oxygen supply and total or protein-bound MDA were observed in only halothane inhaled group. These findings suggested that the cause of halothane-induced hepatopathy is closely related to free radicals mainly generated from halothane anaerobic metabolism under the hypoxic condition. -KEY WORDS: canine, halothane, lipid peroxidation, liver, oxygen supply.
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