School of Civil and Environmental Engineering, Georgia Institute of Technology, 200 Bobby Dodd Way, Atlanta, Georgia 30332, United States.
Environ Sci Technol. 2011 Nov 15;45(22):9627-33. doi: 10.1021/es202269r. Epub 2011 Oct 27.
Motivated by recent studies that documented changes in fullerene toxicity after chemical transformation, C(60) aggregates (nC(60)) were subject to UVC irradiation at monochromatic 254 nm and subsequently evaluated for antibacterial and bactericidal properties against Escherichia coli. The nC(60) treated with UVC irradiation, referred to herein as UVC-irradiated C(60), did not directly inhibit bacterial growth at concentrations up to 20 mg/L. In the presence of UVA and visible light, however, UVC-irradiated C(60) rapidly inactivated E. coli, suggesting that photochemical production of reactive oxygen species (ROS) was involved. The use of ROS scavengers and probes determined that hydroxyl radicals were the primary ROS responsible for the E. coli inactivation. Results from protein release, lipid peroxidation, cell permeability, and intracellular enzyme assays suggest that the inactivation mechanism involves UVC-irradiated C(60) diffusing through E. coli cell membrane and producing hydroxyl radicals within the cell. Further study on water-soluble C(60) derivatives and possible transformative processes is, therefore, recommended based on the environmental implications of results presented herein that nC(60) exposed to UVC irradiation is more toxic than parent nC(60).
受近期研究的启发，这些研究记录了富勒烯毒性在化学转化后的变化，我们将 C(60) 聚集体（nC(60)) 用 254nm 单色紫外线照射，并随后评估其对大肠杆菌的抗菌和杀菌特性。在此文中，经 UVC 照射处理的 nC(60) 被称为 UVC 照射的 C(60)，在高达 20mg/L 的浓度下，它并没有直接抑制细菌生长。然而，在 UVA 和可见光的存在下，UVC 照射的 C(60) 迅速使大肠杆菌失活，这表明光化学反应产生了活性氧物种（ROS）。使用 ROS 清除剂和探针表明，羟基自由基是导致大肠杆菌失活的主要 ROS。从蛋白质释放、脂质过氧化、细胞通透性和细胞内酶测定的结果表明，失活机制涉及 UVC 照射的 C(60) 通过大肠杆菌细胞膜扩散，并在细胞内产生羟基自由基。基于本文提出的结果对环境的影响，建议进一步研究水溶性 C(60) 衍生物和可能的转化过程，因为暴露于 UVC 照射的 nC(60) 比原始的 nC(60) 毒性更大。
