Research Reactor Institute, Kyoto University, Kumatori-cho, Sennan-gun, Osaka 590-0494, Japan.
Mutat Res. 2010 Jan;695(1-2):69-74. doi: 10.1016/j.mrgentox.2009.12.002. Epub 2009 Dec 16.
PURPOSE: Evidence from in vivo studies suggests there are enhanced radiation effects in abscopal regions after local head gamma ray irradiation. Splenocyte apoptosis and T lymphocyte micronuclei were induced at higher rates than what would be estimated given the dose at a shielded, distant position. In addition, we evaluated the radio-protective effects of ascorbic acid, acting as a radical scavenger on enhanced radiation effects in the shielded spleen following local head irradiation. METHODS AND MATERIALS: The heads of C3H mice were exposed to gamma-rays (10-20Gy), while the other parts of the body were shielded with a 5cm-thick lead block. The effective dose for the spleen was calculated at 1.0-2.0Gy. Splenocytes were isolated 24h after cranial irradiation and their apoptosis was measured with an Elisa kit (Roche). The induction of T lymphocyte micronuclei was studied using the cytokinesis-block micronucleus assay. The ascorbic acid glucoside, 2-O-alpha-d-glucopyranosyl-l-ascorbic acid (AA-2G), was orally administered to mice 1h before whole body irradiation. The radio protective effects of AA-2G were estimated by comparing the induction of splenocyte damage (by apoptosis) and micronucleus induction. RESULTS: The splenocyte damage, as measured by the above two methods, was more excessive than what would be expected given exposure to 1.0-2.0Gy of radiation. Our results suggest that the effects were enhanced in a distant, non-irradiated organ after localized irradiation. Plasma ascorbic acid concentrations were increased 8-10x over control. Treatment with ascorbic acid slightly protected mouse splenocytes from the induction of apoptosis by the enhanced effects of radiation in the abscopal region. However, ascorbic acid significantly inhibited micronucleus induction in splenic T lymphocytes following local head irradiation. CONCLUSIONS: Our results suggest that ascorbic acid effectively scavenged radiation-induced radicals and protected against the enhanced effects of radiation in an abscopal region after local head gamma ray irradiation.
目的：体内研究的证据表明，局部头部伽马射线照射后，远隔区的放射效应增强。与屏蔽远处位置的剂量相比，脾细胞凋亡和 T 淋巴细胞微核的诱导率更高。此外，我们评估了抗坏血酸作为自由基清除剂对局部头部照射后屏蔽脾脏中增强的放射效应的放射保护作用。
方法和材料：C3H 小鼠的头部暴露于伽马射线（10-20Gy），而身体的其他部位用 5cm 厚的铅块屏蔽。计算脾脏的有效剂量为 1.0-2.0Gy。头部照射后 24 小时分离脾细胞，并使用 ELISA 试剂盒（罗氏）测量其凋亡。使用细胞有丝分裂阻断微核试验研究 T 淋巴细胞微核的诱导。在全身照射前 1 小时，将抗坏血酸葡萄糖苷，2-O-α-D-吡喃葡萄糖基-L-抗坏血酸（AA-2G）经口给予小鼠。通过比较脾细胞损伤（通过凋亡）和微核诱导，评估 AA-2G 的放射保护作用。
结果：上述两种方法测量的脾细胞损伤比暴露于 1.0-2.0Gy 辐射所预期的更为严重。我们的结果表明，在局部照射后，远处未照射的器官中的效应增强。血浆抗坏血酸浓度比对照增加 8-10 倍。用抗坏血酸处理可轻微保护小鼠脾细胞免受远隔区放射增强效应诱导的凋亡。然而，抗坏血酸显著抑制局部头部照射后脾 T 淋巴细胞的微核诱导。
结论：我们的结果表明，抗坏血酸有效清除了辐射诱导的自由基，并在局部头部伽马射线照射后远隔区的放射增强效应中起到了保护作用。
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