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异佛尔酮二甲基丙烯酸酯对中国仓鼠卵巢细胞的细胞毒性机制。

The mechanisms of cytotoxicity of urethane dimethacrylate to Chinese hamster ovary cells.

机构信息

Department of Dentistry and School of Dentistry, National Taiwan University Hospital and National Taiwan University Medical College, No. 1 Chang-Te Street, Taipei, Taiwan.

出版信息

Biomaterials. 2010 Sep;31(27):6917-25. doi: 10.1016/j.biomaterials.2010.05.059. Epub 2010 Jun 25.

Abstract

Monomers released from resin-containing products may cause various adverse effects. Urethane dimethacrylate (UDMA) is a principal resin monomer and also a major component released from various dental resin materials. Thus the toxic effects and mechanisms should be elucidated for improving of its safety use. Here we investigated the effects of UDMA on the growth, cell cycle progression, reactive oxygen species (ROS) production and glutathione (GSH) alteration in CHO-K1 cells, and the preventive effects by antioxidants (NAC and catalase) were also evaluated. UDMA elicited growth inhibition (>0.025 mm) of CHO-K1 cells in a clearly dose-dependent manner. Cell cycle perturbation and ROS overproduction were also observed. A 0.1 mm UDMA-induced S-phase cell cycle arrest and ROS accumulation. Cell apoptosis and necrosis became significant when UDMA concentration was 0.25 mm. GSH depletion occurred at cells treated with 0.25 mm UDMA, a highly cytotoxic concentration at which point myriad cells were under apoptosis or necrosis. Thus GSH depletion can be crucial for the death of CHO-K1 cells. Furthermore NAC (0.5-10 mm) and catalase (250-1000 U/ml) obviously attenuated the UDMA-induced toxicity by reducing ROS generation and cell cycle disturbance, and the effects were dose-related. These results suggest that UDMA toxicity is associated with ROS production, GSH depletion, cell cycle disturbance and cell apoptosis/necrosis.

摘要

从含树脂产品中释放的单体可能会引起各种不良反应。 聚氨酯二甲基丙烯酸酯(UDMA)是主要的树脂单体,也是各种牙科树脂材料释放的主要成分。因此,为了提高其安全使用,应阐明其毒性作用和机制。在这里,我们研究了 UDMA 对 CHO-K1 细胞生长、细胞周期进程、活性氧(ROS)产生和谷胱甘肽(GSH)改变的影响,还评估了抗氧化剂(NAC 和过氧化氢酶)的预防作用。UDMA 以明显的剂量依赖性方式引起 CHO-K1 细胞生长抑制(>0.025mm)。还观察到细胞周期扰动和 ROS 过度产生。0.1mm UDMA 诱导 S 期细胞周期阻滞和 ROS 积累。当 UDMA 浓度为 0.25mm 时,细胞凋亡和坏死变得明显。当用 0.25mm UDMA 处理时,GSH 耗竭发生,这是一个高度细胞毒性的浓度,此时许多细胞处于凋亡或坏死状态。因此,GSH 耗竭可能对 CHO-K1 细胞的死亡至关重要。此外,NAC(0.5-10mm)和过氧化氢酶(250-1000U/ml)通过减少 ROS 产生和细胞周期紊乱明显减轻了 UDMA 诱导的毒性,并且作用呈剂量依赖性。这些结果表明,UDMA 毒性与 ROS 产生、GSH 耗竭、细胞周期紊乱和细胞凋亡/坏死有关。

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