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首页> 外文会议>Conference on Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XII Jan 25-26, 28, 2003 San Jose, California, USA >Hyperoxygenation Enhances the Direct Tumor Cell Killing of Photofrin-Mediated Photodynamic Therapy
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Hyperoxygenation Enhances the Direct Tumor Cell Killing of Photofrin-Mediated Photodynamic Therapy

机译：过氧化作用增强了光敏蛋白介导的光动力疗法对肿瘤细胞的直接杀伤作用。

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摘要

Tumor hypoxia, either pre-existing or as a result of oxygen bleaching during Photodynamic Therapy (PDT) light irradiation, can significantly reduce the effectiveness of PDT induced cell killing. To overcome the effect of tumor hypoxia and improve tumor cell killing, we propose using supplemental hyperoxygenation during Photofrin PDT. Our previous study has demonstrated that, in an in vivo model, tumor control can be improved by normobaric or hyperbaric 100% oxygen supply. The mechanism for the tumor cure enhancement of the hyperoxygenation-PDT combined therapy is investigated in this study by using an in vivo/in vitro technique. A hypoxic tumor model was established by implanting mammary adenocarcinoma (MCA) in hind legs of C3H mice. Light irradiation (200 J/cm~2 at either 75 or 150 mW/cm~2), under various oxygen supplemental conditions (room air or carbogen or 100% normobaric or hyperbaric 100% oxygen), was delivered through an optical fiber with a microlens to animals who received 12.5 mg/kg Photofrin 24 hours prior to light irradiation. Tumors treated with PDT were harvested and grown in vitro for colony formation analysis. Treated tumors were also analyzed histologically. The results show that, when combined with hyperoxygenation, the cell killing rate immediately after a PDT treatment is significantly improved over that treated without hyperoxygenation, suggesting an enhanced direct cell killing. This study further confirms our earlier observation that when a PDT treatment is combined with hyperoxygenation, it can be more effective in controlling hypoxic tumors. H&E stain revealed that PDT induced tumor necrosis and hemorrhage. In conclusion, by using an in vivo/in vitro assay, we have shown that PDT combined with hyper-oxygenation can enhance direct cell killing and improve tumor cure.
机译：肿瘤缺氧，无论是预先存在的还是在光动力疗法（PDT）光照射过程中由于氧漂白而导致的，都会明显降低PDT诱导的细胞杀伤的效率。为了克服肿瘤缺氧的影响并改善肿瘤细胞的杀伤力，我们建议在Photofrin PDT期间使用补充性超氧合。我们以前的研究表明，在体内模型中，常压或高压100％的氧气供应可以改善肿瘤控制。本研究通过体内/体外技术研究了高氧-PDT联合疗法增强肿瘤治愈的机制。通过将乳腺腺癌（MCA）植入C3H小鼠的后腿来建立缺氧肿瘤模型。通过各种氧气补充条件（室内空气或碳气或100％常压或高压100％氧气）的光照射（在75或150 mW / cm〜2时为200 J / cm〜2）通过具有在光照前24小时接受12.5 mg / kg Photofrin的动物的微透镜。收获用PDT治疗的肿瘤，并在体外生长以进行菌落形成分析。还对治疗的肿瘤进行了组织学分析。结果表明，与高氧结合时，PDT处理后立即的细胞杀灭率显着高于未进行高氧处理的细胞杀灭率，表明直接细胞杀灭能力增强。这项研究进一步证实了我们较早的观察结果，即当PDT治疗与高氧联合使用时，它在控制缺氧肿瘤方面可能更有效。 H＆E染色显示，PDT可诱发肿瘤坏死和出血。总之，通过使用体内/体外试验，我们显示了PDT与高氧合可以增强直接杀伤细胞并改善肿瘤治愈的能力。

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