Ho Yung-Chuan, Huang Fu-Mei, Chang Yu-Chao
School of Applied Chemistry, Chung Shan Medical University, Taichung, Taiwan.
J Biomed Mater Res B Appl Biomater. 2007 Nov;83(2):340-4. doi: 10.1002/jbm.b.30801.
Formaldehyde that leaches out of formaldehyde-releasing root canal sealers, specifically from setting material extruded into the periapical region may participate in the development of periapical inflammation or the continuation of a pre-existing periapical lesion. However, the effects of formaldehyde on human osteoblasts have not been investigated. The aim of this study was to evaluate the mechanisms of cytotoxicity of formaldehyde on human osteoblastic cell line U2OS in vitro. Cytotoxicity and cell proliferation assays were performed to elucidate the adverse effects of formaldehyde on U2OS cells. Formaldehyde demonstrated a cytotoxic effect to U2OS cells in a dose-dependent manner (p<0.05). The 50% inhibition concentration of formaldehyde was about 3 mM. Formaldehyde also inhibited cell proliferation during a 3-day culture period (p<0.05). To determine whether glutathione (GSH) levels were important in the cytotoxicity of formaldehyde, we pretreated cells with the GSH precursor, 2-oxothiazolidine-4-carboxylic acid (OTZ) to boost thiol levels, or buthionine sulfoximine (BSO) to deplete GSH. The addition of OTZ acted as a protective effect on the formaldehyde-induced cytotoxicity (p<0.05). In contrast, the addition of BSO enhanced the formaldehyde-induced cytotoxicity (p<0.05). Taken together, the levels of formaldehyde tested inhibited cell growth and proliferation on U2OS cells. Formaldehyde has significant potential for periapical toxicity. These inhibitory effects were associated with intracellular GSH levels.
从释放甲醛的根管封闭剂中渗出的甲醛，特别是从挤出到根尖周区域的凝固材料中渗出的甲醛，可能参与根尖周炎症的发展或已存在的根尖周病变的持续。然而，甲醛对人成骨细胞的影响尚未得到研究。本研究的目的是在体外评估甲醛对人成骨细胞系U2OS的细胞毒性机制。进行细胞毒性和细胞增殖试验以阐明甲醛对U2OS细胞的不利影响。甲醛对U2OS细胞表现出剂量依赖性的细胞毒性作用（p<0.05）。甲醛的50%抑制浓度约为3 mM。甲醛在3天的培养期内也抑制细胞增殖（p<0.05）。为了确定谷胱甘肽（GSH）水平在甲醛细胞毒性中是否重要，我们用GSH前体2-氧代噻唑烷-4-羧酸（OTZ）预处理细胞以提高硫醇水平，或用丁硫氨酸亚砜胺（BSO）消耗GSH。添加OTZ对甲醛诱导的细胞毒性起到保护作用（p<0.05）。相反，添加BSO增强了甲醛诱导的细胞毒性（p<0.05）。综上所述，所测试的甲醛水平抑制了U2OS细胞的生长和增殖。甲醛具有显著的根尖周毒性潜力。这些抑制作用与细胞内GSH水平有关。
