Protective effect of sulphoraphane against oxidative stress mediated toxicity induced by CuO nanoparticles in mouse embryonic fibroblasts BALB 3T3
Protective effect of sulphoraphane against oxidative stress mediated toxicity induced by CuO nanoparticles in mouse embryonic fibroblasts BALB 3T3
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DOI：
10.2131/jts.37.139
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发表时间：
2012-02-01
影响因子：
2
通讯作者：
Kumar, Sudhir
中科院分区：
文献类型：
--
作者：
Akhtar, Mohd Javed;Ahamed, Maqusood;Kumar, Sudhir
尽管人们对纳米颗粒（NP）的安全性非常感兴趣，但尚未开发出全面的测试范例。氧化应激被认为是纳米粒子毒性背后的一个解释。据报道，花椰菜和西兰花等十字花科蔬菜中存在的萝卜硫素（SFN）具有保护细胞免受氧化损伤和炎症的潜力。然而，SFN 在纳米毒性中的保护作用尚未探讨。我们研究了 SFN 对小鼠胚胎成纤维细胞 (BALB 3T3) 中氧化铜 (CuO) 纳米颗粒毒性反应的保护作用。结果表明，MTT 和乳酸脱氢酶 (LDH) 测定表明，CuO NPs 在 BALB 3T3 细胞中诱导剂量依赖性 (5-15 μg/ml) 细胞毒性。 CuO NPs 还被发现以剂量依赖性方式诱导氧化应激，表现为活性氧 (ROS) 和脂质过氧化 (LPO) 的诱导以及谷胱甘肽和谷胱甘肽还原酶的消耗。 BALB 3T3 细胞与 SFN (6 μM) 共同处理显着减弱了 CuO NPs 引起的细胞毒性、ROS 产生和氧化应激。此外，我们发现另一种抗氧化剂 N-乙酰半胱氨酸 (NAC) (2 mM) 的共同处理也显着减弱了 CuO NP 引起的谷胱甘肽消耗，但对 CuO NP 暴露导致的细胞活力丧失的保护并不显着。我们相信这是第一份表明 SFN 显着保护 BALB 3T3 细胞免受 CuO NP 毒性的报告，这种毒性是通过氧化剂的产生和抗氧化剂的消耗来介导的。因此，SFN 对 CuO NPs 毒性的保护机制与 NAC 不同，应进一步研究。
Despite the great interest in nanoparticles (NPs) safety, no comprehensive test paradigm has been developed. Oxidative stress has been implicated as an explanation behind the toxicity of NPs. It is reported that sulphoraphane (SFN) present in cruciferous vegetables like cauliflower and broccoli has potential to protect cells from oxidative damage and inflammation. However, protective role of SFN in nanotoxicity is not explored. We investigated the protective effect of SFN against the toxic response of copper oxide (CuO) NPs in mouse embryonic fibroblasts (BALB 3T3). Results showed that CuO NPs induced dose-dependent (5-15 mu g/ml) cytotoxicity in BALB 3T3 cells demonstrated by MTT and lactate dehydrogenase (LDH) assays. CuO NPs were also found to induce oxidative stress in dose-dependent manner indicated by induction of reactive oxygen species (ROS) and lipid peroxidation (LPO) and depletion of glutathione and glutathione reductase. Co-treatment of BALB 3T3 cells with SFN (6 mu M) significantly attenuated the cytotoxicity, ROS generation and oxidative stress caused by CuO NPs. Moreover, we found that co-treatment of another antioxidant N-acetyl-cysteine (NAC) (2 mM) also significantly attenuated glutathione depletion caused by CuO NPs but protection from the loss of cell viability due to CuO NPs exposure was not significant. We believe this is the first report showing that SFN significantly protected the BALB 3T3 cells from CuO NPs toxicity, which is mediated through generation of oxidants and depletion of antioxidants. Consequently, protective mechanism of SFN against CuO NPs toxicity was different from NAC that should be further investigated.