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目的游离脂肪酸可与铁结合并转运铁进入细胞,而人们对游离脂肪酸与铁诱发的突变和DNA损伤的潜在协同作用知之甚少。方法该文研究了铁和游离脂肪酸的协同毒性作用,在成纤维细胞中通过HPRT基因突变测量其潜在致突变作用,并通过8羟基脱氧鸟苷的形成测量对DNA的损伤。同时还研究了铁和游离脂肪酸介导的线粒体功能障碍。结果结果发现铁和游离脂肪酸的组合在成纤维细胞中有明显的协同毒性作用,而单独的铁和游离脂肪酸不显示任何影响。铁和游离脂肪酸的组合能明显增加活性氧自由基的产生,产生显著的HPRT突变,DNA损伤,以及线粒体功能障碍。结论游离脂肪酸和铁可以发挥协同的细胞毒性,在哺乳动物细胞中增加活性氧自由基的产生,导致HPRT突变,DNA损伤与线粒体功能障碍。由于与铁的协同毒性作用,游离脂肪酸对人体健康可能是一个潜在的危险因素。
The purpose of free fatty acids can bind to iron and transport iron into cells, and little is known about the potential synergy between free fatty acids and iron-induced mutations and DNA damage. METHODS: The synergistic toxic effects of iron and free fatty acids were studied in this paper. Potential mutagenicity was measured in fibroblasts by HPRT gene mutation and DNA damage was measured by the formation of 8-hydroxy-deoxyguanosine. Iron and free fatty acid-mediated mitochondrial dysfunction were also studied. As a result, it was found that the combination of iron and free fatty acid showed a significant synergistic toxic effect in fibroblasts, while iron and free fatty acids alone did not show any effect. The combination of iron and free fatty acids can significantly increase reactive oxygen species production, resulting in significant HPRT mutations, DNA damage, and mitochondrial dysfunction. Conclusions Both free fatty acids and iron exert synergistic cytotoxicity and increase reactive oxygen species in mammalian cells, resulting in HPRT mutations, DNA damage and mitochondrial dysfunction. Due to the synergistic toxicity with iron, free fatty acids may be a potential risk factor for human health.