Ogawa Yasuhiro, Takahashi Toshiaki, Kobayashi Toshihiro, Kariya Shinji, Nishioka Akihito, Mizobuchi Hiroo, Noguchi Masataka, Hamasato Shinji, Tani Toshikazu, Seguchi Harumichi, Yoshida Shoji, Sonobe Hiroshi
Department of Radiology, Kochi Medical School, Oko-cho, Nankoku-shi, Kochi-Prefecture 783-8505, Japan.
Int J Mol Med. 2003 Oct;12(4):453-8.
In our previous study, we examined reactive oxygen species (ROS) formation in T lymphocytes following 5 Gy of irradiation. Using a CCD camera system, we monitored fluorescence in T lymphocytes loaded with the succinimidyl ester of Dichlorodihydrofluorescein diacetate (H2DCFDA), which is non-fluorescent until oxidized by ROS. We found that ROS formation occurred immediately after irradiation, continued for several hours, and resulted in oxidative DNA damage. Therefore, the origin of the hyper-radiosensitivity of T lymphocytes seemed to be the high production of ROS in the mitochondrial DNA following irradiation. In this study, we examined radiation-induced ROS formation, oxidative DNA damage, early apoptotic changes, and mitochondrial membrane dysfunction in the human osteosarcoma cell line HS-Os-1, which was established from an osteoblastic tumor that arose in the left humerus of an 11-year-old girl and was already morphologically characterized in vitro and in vivo. We found that ROS formation and oxidative DNA damage were actually scarcely seen after irradiation of up to 30 Gy in these cells; that mitochondrial membrane potential was preserved; and that apoptotic changes were not demonstrated despite the relatively high-dose irradiation of 30 Gy. Therefore, the origin of the close similarity of radiosensitivity between adult articular chondrocytes and the human osteosarcoma cell line HS-Os-1, is considered to involve the low degree of ROS formation following irradiation; the similarity possibly results from the strong scavenging ability of these two kinds of cells for free radicals including hydroxyl radicals.
在我们之前的研究中，我们检测了5 Gy照射后T淋巴细胞中活性氧（ROS）的形成。使用电荷耦合器件（CCD）相机系统，我们监测了负载二氯二氢荧光素二乙酸琥珀酰亚胺酯（H2DCFDA）的T淋巴细胞中的荧光，H2DCFDA在被ROS氧化之前是无荧光的。我们发现照射后立即发生ROS形成，并持续数小时，导致氧化性DNA损伤。因此，T淋巴细胞超放射敏感性的起源似乎是照射后线粒体DNA中ROS的高产生。在本研究中，我们检测了人骨肉瘤细胞系HS-Os-1中辐射诱导的ROS形成、氧化性DNA损伤、早期凋亡变化和线粒体膜功能障碍，该细胞系源自一名11岁女孩左肱骨发生的成骨细胞瘤，已在体外和体内进行了形态学特征鉴定。我们发现，在这些细胞中照射高达30 Gy后，实际上几乎看不到ROS形成和氧化性DNA损伤；线粒体膜电位得以保留；尽管进行了30 Gy的相对高剂量照射，但未显示凋亡变化。因此，成人关节软骨细胞和人骨肉瘤细胞系HS-Os-1之间放射敏感性密切相似的起源，被认为与照射后ROS形成程度较低有关；这种相似性可能源于这两种细胞对包括羟基自由基在内的自由基的强大清除能力。
