Kassis A I, Adelstein S J, Mariani G
Department of Radiology, (Division of Nuclear Medicine), Harvard Medical School, Boston, MA 02115, USA.
Q J Nucl Med. 1996 Sep;40(3):301-19.
Radiolabeled nucleosides, specifically 5-iodo-2'-deoxyuridine (IUdR) radioiodinated with the Auger-electronemitting 123I or 125I, have been shown to produce extensive DNA damage in mammalian cell systems in vitro. Such nucleosides are cycle-dependent agents that are taken up by mitotically dividing cells in the S phase of the cell cycle. The degree of damage that occurs is related to the fact that these nucleosides bind covalently to DNA bringing the decaying Augerelectron-emitting radionuclide in close proximity to the genome. The use of these radiohalogenated nucleosides in vivo is associated with several problems. The first relates to their extremely short biologic half-life in blood (T1/2 of minutes in humans). The second involves achieving therapeutic ratios in tumor cells in the face of efficient hepatic dehalogenation. The third concerns the uptake of these radiopharmaceuticals by actively proliferating normal cell renewal systems, thus potentially causing toxic side effects. The fourth, one shared with other cycle-dependent drugs, relates to the matter of labeling the whole tumor cell population. To facilitate targeting to tumors, investigators have been examining the direct introduction of these agents into the targeted area or into an arterial blood supply that immediately precedes the target. For example, radiopharmaceutical administration could be intracavitary (bladder, spinal fluid, peritoneum), intralesional (brain tumor, breast mass) or intra-arterial (liver, pancreas). In all these situations, the following conditions must be met: (a) once within the vicinity of the tumor the agent can freely diffuse through the tissues and is selectively taken up by cancerous cells; (b) once the agent has left the target area it is converted quickly into a nontoxic form and/or excreted from the body; and finally, (c) the biologic behavior of the agent is not altered by repeated injections. We report herein our experience and that of others with [123I/125I/131I]IUdR in cultured cells, animal tumor-model systems, and patients. In vitro, DNA incorporation of 123I- and 125I-labeled IUdR leads to an exponential decrease in cell survival (no shoulder on the survival curve). However, the total number of decays needed to produce a given lethal effect with [123I]IUdR is approximately twice that required with [125I]IUdR. In vivo, the scintigraphic and antineoplastic capabilities of radioiodinated IUdR have been demonstrated in an intraperitoneal murine ovarian tumor model following intraperitoneal injection; in an intracerebral rat gliosarcoma model after intracranial administration; in an intrathecal rat gliosarcoma model after intrathecal infusion; and in a rat transitional cell bladder cancer model following intravesicular infusion. [123I]IUdR, [125I]IUdR, and/or [131I]IUdR have been administered to patients with brain, breast, colorectal, or gastrointestinal cancers (intratumorally); ovarian cancer (intraperitoneally); bladder cancer (intravesically); liver metastases from colorectal cancer (through the hepatic artery, permanent intra-arterial catheter). These studies have confirmed the observations made in animal models. The data indicate that 5-iodo-2'-deoxyuridine radiolabeled with an Auger electron emitter (123I or 125I) may be a useful agent for the scintigraphic diagnosis and/or therapy of neoplastic diseases that are accessible to direct radiopharmaceutical administration. This radiopharmaceutical should serve as a prototype for, and facilitate the development of, other radiolabeled nucleoside analogs. Further investigations are certainly warranted.
放射性标记的核苷,特别是用发射俄歇电子的¹²³I或¹²⁵I进行放射性碘化的5-碘-2'-脱氧尿苷(IUdR),已证实在体外哺乳动物细胞系统中可造成广泛的DNA损伤。这类核苷是细胞周期依赖性药物,在细胞周期的S期被有丝分裂的细胞摄取。所发生的损伤程度与这些核苷与DNA共价结合这一事实有关,从而使衰变的发射俄歇电子的放射性核素靠近基因组。在体内使用这些放射性卤代核苷存在几个问题。第一个问题与它们在血液中极短的生物半衰期有关(在人类中为几分钟的T₁/₂)。第二个问题涉及在肝脏有效脱卤的情况下在肿瘤细胞中实现治疗比率。第三个问题是这些放射性药物被活跃增殖的正常细胞更新系统摄取,从而可能导致毒副作用。第四个问题与其他细胞周期依赖性药物共有的问题,涉及标记整个肿瘤细胞群体。为便于靶向肿瘤,研究人员一直在研究将这些药物直接引入靶区或引入紧接靶区之前的动脉血供中。例如,放射性药物给药可以是腔内给药(膀胱、脑脊液、腹膜)、瘤内给药(脑肿瘤、乳腺肿块)或动脉内给药(肝脏、胰腺)。在所有这些情况下,必须满足以下条件:(a)一旦在肿瘤附近,药物能够自由扩散通过组织并被癌细胞选择性摄取;(b)一旦药物离开靶区,它会迅速转化为无毒形式和/或从体内排出;最后,(c)药物的生物学行为不会因重复注射而改变。我们在此报告我们以及其他人在培养细胞、动物肿瘤模型系统和患者中使用[¹²³I/¹²⁵I/¹³¹I]IUdR的经验。在体外,¹²³I和¹²⁵I标记的IUdR掺入DNA导致细胞存活率呈指数下降(存活曲线上无肩区)。然而,用[¹²³I]IUdR产生给定致死效应所需的衰变总数约为用[¹²⁵I]IUdR所需衰变总数的两倍。在体内,放射性碘化的IUdR的闪烁显像和抗肿瘤能力已在腹腔内注射后的腹腔内小鼠卵巢肿瘤模型、颅内给药后的脑内大鼠胶质肉瘤模型、鞘内输注后的鞘内大鼠胶质肉瘤模型以及膀胱内输注后的大鼠移行细胞膀胱癌模型中得到证实。[¹²³I]IUdR、[¹²⁵I]IUdR和/或[¹³¹I]IUdR已被给予患有脑癌、乳腺癌、结直肠癌或胃肠道癌的患者(瘤内给药);卵巢癌患者(腹腔内给药);膀胱癌患者(膀胱内给药);结直肠癌肝转移患者(通过肝动脉、永久性动脉内导管)。这些研究证实了在动物模型中所做的观察。数据表明,用俄歇电子发射体(¹²³I或¹²⁵I)放射性标记的5-碘-2'-脱氧尿苷可能是一种对可直接进行放射性药物给药的肿瘤疾病进行闪烁显像诊断和/或治疗的有用药物。这种放射性药物应作为其他放射性标记核苷类似物的原型并促进其开发。进一步的研究当然是必要的。