Geraniol (GOH), like other plant-derived natural bioactive compounds, has been found to possess antiproliferative properties that are essential to cope with malignant tumors. However, the mechanisms of molecular action are not fully elucidated. The aim of this study was to evaluate the effect of GOH on some oxidative parameters in human tumor cell lines (HepG2 and A549). Cytotoxicity evaluated in cell lines by the MTT assay, genotoxicity by the comet assay, and lipid peroxidation by the TBARS. The activities of antioxidant the enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST), were also analyzed. Additionally, intracellular reactive oxygen species (ROS), nitric oxide, and lactate production were determined in HepG2 cells. Both tumor cell lines showed a clear concentration-dependent response to GOH in several of the parameters evaluated. Lipids turned out to be more sensitive than DNA to oxidative damage induced by GOH. TBARS levels increased with respect to control (p < 0.05) by 33% and 122% in HepG2 and A549 cells, respectively treated with 200 μM GOH. However, GOH caused a statistically significant decrease in SOD and CAT activities in HepG2 cells only. GST was not affected in any cell lines. GOH induced the production of ROS but not nitric oxide in HepG2, which shows that ROS were mainly responsible for oxidative damage. Lactate release increased statistically significantly compared to control (p < 0.001), by 41% and 86% at 200 and 800 μM GOH respectively, showing that this monoterpene also affected the glycolytic pathway in HepG2 cells. These results suggest that oxidative stress could mediate the anti-proliferative effects of GOH in HepG2 and A549 cells.

中文翻译：

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氧化应激的诱导是香叶醇影响人A549和HepG2肿瘤细胞增殖的可能机制。

与其他植物来源的天然生物活性化合物一样，香叶醇（GOH）也具有抗增殖特性，这些特性对于应对恶性肿瘤至关重要。但是，分子作用的机理尚未完全阐明。这项研究的目的是评估GOH对人肿瘤细胞系（HepG2和A549）某些氧化参数的影响。通过MTT分析评估细胞系的细胞毒性，通过彗星分析评估基因毒性，并通过TBARS评估脂质过氧化作用。还分析了抗氧化剂的酶，超氧化物歧化酶（SOD），过氧化氢酶（CAT）和谷胱甘肽-S-转移酶（GST）的活性。此外，在HepG2细胞中测定了细胞内活性氧（ROS），一氧化氮和乳酸的产生。在所评估的几个参数中，两种肿瘤细胞系均显示出对GOH的明显的浓度依赖性反应。事实证明，脂质比DNA对GOH引起的氧化损伤更敏感。分别用200μMGOH处理的HepG2和A549细胞中，TBARS水平相对于对照增加（p <0.05）33％和122％。然而，仅在HepG2细胞中，GOH引起了SOD和CAT活性的统计学显着下降。GST在任何细胞系中均不受影响。GOH诱导了HepG2中ROS的产生，但不引起一氧化氮的产生，这表明ROS主要负责氧化损伤。与对照相比，乳酸释放在统计学上显着增加（p <0.001），分别在200和800μMGOH时分别增加41％和86％，表明该单萜还影响HepG2细胞中的糖酵解途径。