The cytotoxicity of methacrylate-based biopolymers crosslinked by in situ photopolymerization has been attributed mainly to residual methacrylate monomers released due to incomplete polymerization. The residual monomers, primarily triethyleneglycol dimethacrylate or 2-hydroxyethyl methacrylate, may irritate adjacent tissue, or be released into the bloodstream and reach practically all tissues. Increased production of reactive oxygen species, which may be connected to concomitant glutathione depletion, has been the most noticeable effect observed in vitro following the exposure of cells to methacrylates. Radical scavengers such as glutathione or N-acetylcysteine represent the most important cellular strategy against methacrylate-induced toxicity by direct adduct formation, resulting in monomer detoxification. Reactive oxygen species may participate in methacrylate-induced genotoxic or pro-apoptotic effects and cell-cycle arrest via induction of corresponding molecular pathways in cells. A deeper understanding of the biological mechanisms and effects of methacrylates widely used in various bioapplications may enable a better estimation of potential risks and thus, selection of a more appropriate composition of polymer material to eliminate potentially harmful substances such as triethyleneglycol dimethacrylate.

中文翻译：

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阐明生物材料中使用的甲基丙烯酸酯单体潜在毒性的细胞和分子机理。

通过原位光聚合交联的基于甲基丙烯酸酯的生物聚合物的细胞毒性主要归因于由于聚合不完全而释放的残留甲基丙烯酸酯单体。残留的单体，主要是二甲基丙烯酸三乙二醇酯或甲基丙烯酸2-羟乙酯，可能刺激附近的组织，或释放到血流中并到达几乎所有组织。细胞暴露于甲基丙烯酸酯后，在体外观察到的最明显的作用是增加了活性氧的产生，这可能与谷胱甘肽的伴随消耗有关。自由基清除剂，例如谷胱甘肽或N-乙酰半胱氨酸代表了最重要的细胞策略，可通过直接形成加合物来抵抗甲基丙烯酸酯诱导的毒性，从而导致单体解毒。活性氧可通过诱导细胞中相应的分子途径参与甲基丙烯酸酯诱导的遗传毒性或促凋亡作用以及细胞周期停滞。对在各种生物应用中广泛使用的甲基丙烯酸酯的生物学机理和作用的更深入了解，可以更好地估计潜在风险，因此可以选择一种更合适的聚合物材料成分来消除潜在的有害物质，例如三乙二醇二甲基丙烯酸酯。