Department of Zoology, Mizoram University, Aizawl, India.
Int J Radiat Biol. 2021;97(4):485-493. doi: 10.1080/09553002.2021.1876948. Epub 2021 Feb 2.
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.
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 Co 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.
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.
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.
电离辐射会引发自由基的形成，从而破坏 DNA 并导致细胞死亡。微核试验可以简单地评估 DNA 损伤，而阻碍自由基形成的药效团则可以有效降低辐照引起的 DNA 损伤。因此，本研究旨在确定姜黄素减轻人外周血淋巴细胞（HPBLs）暴露于 0-4Gyγ 射线后微核形成的能力。
将 HPBLs 用 0.125、0.25、0.5、1、2、5、10、20 或 50μg/mL 姜黄素处理 30 分钟后，再用 3Gyγ 射线照射；或用 0.5μg/mL 姜黄素在 0、0.5、1、2、3 或 4Gy Coγ 辐照前 30 分钟处理，阻断 HPBLs 的细胞分裂，并计算微核。采用标准方法测定姜黄素体外抑制自由基诱导的能力。
3Gy 辐照前用不同浓度姜黄素处理的 HPBLs 减轻了微核的形成，且与单独 3Gy 辐照相比，在 0.5μg/mL 姜黄素时微核最少。随着姜黄素浓度的增加，微核逐渐增加，在 10-50μg/mL 姜黄素时比单独 3Gy 辐照显著增加。HPBLs 用不同剂量的γ射线照射后，微核明显增加，而用 0.5μg/mL 姜黄素在照射前 30 分钟处理不同剂量的γ射线后，具有一个、两个或更多微核的 HPBLs 频率显著降低。姜黄素处理呈浓度依赖性地抑制羟自由基（OH）、2,2-偶氮-双（3-乙基苯并噻唑啉-6-磺酸）（ABTS）、2,2-二苯基-1-苦肼基（DPPH）和（一氧化氮）NO 自由基的形成。
姜黄素在 0.5μg/mL 的剂量下处理可通过抑制辐射诱导自由基的形成来减轻 γ 射线照射后的微核形成。
