School of Public Health, Medical College, Wuhan University of Science and Technology, Wuhan, 430081, Hubei, China.
J Appl Toxicol. 2013 Dec;33(12):1468-73. doi: 10.1002/jat.2814. Epub 2012 Oct 12.
Formaldehyde is ubiquitous in the environment. It is known to be a genotoxic substance. We hypothesized that reactive oxygen species (ROS) and lipid peroxidation are involved in formaldehyde-induced genotoxicity in human lung cancer cell lines A549. To test this hypothesis, we investigated the effects of antioxidant on formaldehyde-induced genotoxicity in A549 Cell Lines. Formaldehyde exposure caused induction of DNA-protein cross-links (DPCs). Curcumin is an important antioxidant. Formaldehyde significantly increased malondialdehyde (MDA) levels, and decreased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity. In addition, the activation of NF-κB and AP-1 were induced by formaldehyde treatment. Pretreatment with curcumin counteracted formaldehyde-induced oxidative stress, ameliorated DPCs and attenuated activation of NF-κB and AP-1 in A549 Cell Lines. These results, taken together, suggest that formaldehyde induced genotoxicity through its ROS and lipid peroxidase activity and caused DPCs effects in A549 cells.
甲醛在环境中无处不在。它是一种已知的遗传毒性物质。我们假设活性氧（ROS）和脂质过氧化与甲醛诱导的人肺癌细胞系 A549 中的遗传毒性有关。为了验证这一假设，我们研究了抗氧化剂对 A549 细胞系中甲醛诱导的遗传毒性的影响。甲醛暴露导致 DNA-蛋白质交联（DPCs）的诱导。姜黄素是一种重要的抗氧化剂。甲醛显著增加丙二醛（MDA）水平，并降低超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）活性。此外，甲醛处理诱导 NF-κB 和 AP-1 的激活。用姜黄素预处理可拮抗甲醛诱导的氧化应激，减轻 A549 细胞中的 DPCs 并减弱 NF-κB 和 AP-1 的激活。这些结果表明，甲醛通过其 ROS 和脂质过氧化活性诱导遗传毒性，并在 A549 细胞中引起 DPCs 效应。
