School of Public Health and Institute of Health and Environment, Seoul National University, Seoul, Republic of Korea.
Drug Chem Toxicol. 2011 Jul;34(3):277-84. doi: 10.3109/01480545.2010.546800.
The phototoxicity of ultraviolet A irradiation (UVA) can be enhanced by photosensitizing agents, such as titanium dioxide nanoparticles (100 nm in diameter, "normal-TiO₂"). Nano-TiO₂ treatment in the absence of UVA caused a slight decrease in cell viability, but in the presence of UVA, it caused a significant decrease in cell viability. In the presence of UVA, nano-TiO₂ also significantly increased the percentage of the cell population in the sub-G₁ phase, induced activation of the proapoptotic proteins, caspase-9, caspase-3, and poly(ADP)ribose polymerase, significantly increased the production of reactive oxygen species (ROS), and induced the loss of the mitochondrial membrane potential (MMP), suggesting that UVA and nano-TiO₂ synergistically promoted apoptosis via a mitochondrial pathway. In the presence of UVA, but not in its absence, nano-TiO₂ treatment also caused a significant increase in DNA damage. Normal-TiO₂ used at the same concentrations did not cause DNA damage, induce ROS generation, trigger mitochondrial membrane depolarization, or increase apoptotic cell death, regardless of UVA exposure. Taken together, these results suggest that nano-TiO₂ and UVA synergistically promote rapid ROS generation and MMP collapse, triggering apoptosis. Additionally, they show that small TiO₂ particles are more phototoxic than larger ones.
紫外 A 辐射（UVA）的光毒性可以通过光敏剂增强，例如二氧化钛纳米颗粒（直径 100nm，“普通-TiO₂”）。在没有 UVA 的情况下，纳米 TiO₂处理会导致细胞活力略有下降，但在存在 UVA 的情况下，会导致细胞活力显著下降。在存在 UVA 的情况下，纳米 TiO₂还会显著增加处于 sub-G₁ 期的细胞群体百分比，诱导促凋亡蛋白、半胱天冬酶-9、半胱天冬酶-3 和多聚（ADP-核糖）聚合酶的激活，显著增加活性氧（ROS）的产生，并诱导线粒体膜电位（MMP）的丧失，表明 UVA 和纳米 TiO₂通过线粒体途径协同促进细胞凋亡。在存在 UVA 的情况下，但不存在 UVA 的情况下，纳米 TiO₂处理也会导致 DNA 损伤显著增加。相同浓度的普通-TiO₂不会导致 DNA 损伤、诱导 ROS 生成、触发线粒体膜去极化或增加凋亡细胞死亡，无论是否暴露于 UVA。总之，这些结果表明，纳米 TiO₂和 UVA 协同促进快速 ROS 生成和 MMP 崩溃，引发细胞凋亡。此外，它们表明小的 TiO₂颗粒比大的颗粒更具光毒性。
