Abstract

Purpose

Ionizing radiations trigger the formation of free radicals that damage DNA and cause cell death. DNA damage may be simply evaluated by micronucleus assay and the pharmacophores that impede free radicals could effectively reduce the DNA damage initiated by irradiation. Therefore, it was desired to determine the capacity of curcumin to alleviate micronuclei formation in human peripheral blood lymphocytes (HPBLs) exposed to 0–4 Gy of γ-radiation.

Materials and methods

HPBLs were exposed to 3 Gy after 30 minutes of 0.125, 0.25, 0.5, 1, 2, 5, 10, 20 or 50 µg/mL curcumin treatment or with 0.5 μg/mL curcumin 30 minutes early to 0, 0.5, 1, 2, 3 or 4 Gy ⁶⁰Co γ-irradiation. Cytokinesis of HPBLs was blocked by cytochalasin B and micronuclei scored. The ability of curcumin to suppress free radical induction in vitro was determined by standard methods.

Results

HPBLs treated with different concentrations of curcumin before 3 Gy irradiation alleviated the micronuclei formation depending on curcumin concentration and the lowest micronuclei were detected at 0.5 µg/mL curcumin when compared to 3 Gy irradiation alone. Increasing curcumin concentration caused a gradual rise in micronuclei, and the significant increases were detected at 10–50 µg/mL curcumin than 3 Gy irradiation alone. Irradiation of HPBLs to different doses of γ-rays caused a significant rise in micronuclei depending on radiation dose, whereas HPBLs treated with 0.5 µg/mL curcumin 30 minutes before irradiation to different doses of γ-rays significantly reduced frequencies of HPBLs with one, two, or more micronuclei. Curcumin treatment inhibited the formation of hydroxyl (OH), 2,2-azinobis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS), 2,2′-diphenyl-1-picrylhydrazyl (DPPH), and (nitric oxide) NO free radicals in a concentration-related way.

Conclusions

Curcumin when treated at a dose of 0.5 μg/mL attenuated micronuclei formation after γ-irradiation by inhibiting the formation of radiation-induced free radicals.

中文翻译：

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姜黄素的抗氧化活性可防止暴露于各种剂量γ-辐射的培养的人外周血淋巴细胞中辐射诱导的微核形成

摘要

目的

电离辐射会引发自由基的形成，自由基会损害 DNA 并导致细胞死亡。DNA 损伤可以简单地通过微核试验来评估，并且阻碍自由基的药效团可以有效地减少由辐射引发的 DNA 损伤。因此，需要确定姜黄素减轻暴露于 0-4 Gy γ 辐射的人外周血淋巴细胞 (HPBLs) 微核形成的能力。

材料和方法

HPBLs 在 0.125、0.25、0.5、1、2、5、10、20 或 50 µg/mL 姜黄素处理 30 分钟后或使用 0.5 µg/mL 姜黄素处理 30 分钟后暴露于 3 Gy，提前 30 分钟至 0、0.5、1、2 , 3 或 4 Gy ⁶⁰ Co γ 辐照。HPBLs 的细胞分裂被细胞松弛素 B 阻断，并对微核进行评分。姜黄素在体外抑制自由基诱导的能力是通过标准方法确定的。

结果

在 3 Gy 辐照前用不同浓度的姜黄素处理的 HPBL 根据姜黄素浓度减轻了微核的形成，与单独的 3 Gy 辐照相比，在 0.5 µg/mL 姜黄素时检测到最低的微核。增加姜黄素浓度导致微核逐渐增加，在 10–50 µg/mL 姜黄素时检测到比单独 3 Gy 辐射显着增加。用不同剂量的 γ 射线照射 HPBLs 会导致微核显着增加，这取决于辐射剂量，而在照射不同剂量的 γ 射线前 30 分钟用 0.5 µg/mL 姜黄素处理的 HPBLs 显着降低了 HPBLs 的频率，1、2 ，或更多的微核。姜黄素处理抑制了羟基 (OH), 2,2-azinobis(3-ethylbenzothiazoline-6-sulfonic acid, ABTS), 2,

结论

姜黄素以 0.5 μg/mL 的剂量处理时，通过抑制辐射诱导的自由基的形成，减弱了 γ 辐射后的微核形成。