Grupo de Investigaciones Básicas y Aplicadas en Odontología, Departamento de Salud Oral, Universidad Nacional de Colombia, Bogotá, Colombia.
Grupo de Virología, Universidad El Bosque, Bogotá, Colombia.
Chem Biol Interact. 2021 Jan 5;333:109336. doi: 10.1016/j.cbi.2020.109336. Epub 2020 Nov 25.
Resin-based dental materials consist of filler particles and different monomers that are light cured in situ to re-establish dental function and aesthetics. Due to the degree of conversion of adhesive polymers, the monomers triethyleneglycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) are released in relatively high amounts and are susceptible to degradation, acting as bioactive compounds and affecting cell and tissues. This study aimed to assess the effect of HEMA and TEGDMA exposure on metabolic activity, membrane integrity, and cell survival of human odontoblast-like cell (hOLCs). Exposure to resin monomers for 24 h induced major changes in cell membrane integrity, metabolic activity, and survival, which were measured by the calcein method and lactate dehydrogenase release. Increased and early reactive oxygen species (ROS) production was observed leading to degradative oxidation of membrane lipids identified as malondialdehyde production. Severe alteration in mitochondria occurred due to transmembrane mitochondrial potential collapse, possibly inducing activation of apoptotic cell death. hOLCs exposure to resin monomers modified the cell redox potential, with consequences on membrane permeability and integrity, including mitochondrial function. Lipid peroxidation appears to be a key phenomenon for the membrane structures oxidation after HEMA and TEGDMA exposure, leading to cell death and cytotoxicity. hOLCs respond early by differential induction of adaptive mechanisms to maintain cell homeostasis. Modulation of oxidative stress-induced response involves the regulation of genes that encode for antioxidant proteins such as catalase and heme oxygenase-1; regulation that functions as a critical protection mechanism against oxidative cell damage induced by HEMA and TEGDMA. Ascorbic acid as an antioxidant substance mitigates the oxidative damage associated with exposure to monomers.
树脂基牙科材料由填充颗粒和不同的单体组成，这些单体在原位光固化以恢复牙齿的功能和美观。由于粘合聚合物的转化率，三甘醇二甲基丙烯酸酯（TEGDMA）和 2-羟乙基甲基丙烯酸酯（HEMA）等单体以相对较高的量释放，并容易降解，作为生物活性化合物，影响细胞和组织。本研究旨在评估 HEMA 和 TEGDMA 暴露对人成牙本质样细胞（hOLC）代谢活性、膜完整性和细胞存活的影响。暴露于树脂单体 24 小时会导致细胞膜完整性、代谢活性和存活的重大变化，这可以通过钙黄绿素法和乳酸脱氢酶释放来测量。观察到早期和增加的活性氧（ROS）产生，导致膜脂质的降解氧化，鉴定为丙二醛的产生。由于跨膜线粒体电势崩溃，线粒体发生严重改变，可能诱导细胞凋亡的激活。hOLC 暴露于树脂单体改变了细胞的氧化还原电势，对膜通透性和完整性产生影响，包括线粒体功能。脂质过氧化似乎是 HEMA 和 TEGDMA 暴露后膜结构氧化的关键现象，导致细胞死亡和细胞毒性。hOLC 通过诱导适应性机制来维持细胞内稳态，对细胞内稳态的早期变化做出反应。氧化应激诱导反应的调节涉及调节编码抗氧化蛋白的基因，如过氧化氢酶和血红素加氧酶-1；这种调节作为一种关键的保护机制，防止 HEMA 和 TEGDMA 诱导的氧化细胞损伤。抗坏血酸作为一种抗氧化物质，可以减轻与单体暴露相关的氧化损伤。
