Maurya Dharmendra Kumar, Balakrishnan Sreedevi, Salvi Veena Prakash, Nair Cherupally Krishnan Krishnan
Radiation Biology & Health Sciences Division, Bhabha Atomic Research Centre, Mumbai, 400085, India.
Mol Cell Biochem. 2005 Dec;280(1-2):57-68. doi: 10.1007/s11010-005-8052-3.
The effect of troxerutin on gamma-radiation-induced DNA strand breaks in different tissues of mice in vivo and formations of the micronuclei were studied in human peripheral blood lymphocytes ex vivo and mice blood reticulocytes in vivo. Treatments with 1 mM troxerutin significantly inhibited the micronuclei induction in the human lymphocytes. Troxerutin protected the human peripheral blood leucocytes from radiation-induced DNA strand breaks in a concentration dependent manner under ex vivo condition of irradiation (2 Gy). Intraperitoneal administration of troxerutin (175 mg/kg body weight) to mice before and after whole body radiation exposure inhibited micronuclei formation in blood reticulocytes significantly. The administration of different doses (75, 125 and 175 mg/kg body weight) of troxerutin 1 h prior to 4 Gy gamma-radiation exposure showed dose-dependent decrease in the yield of DNA strand breaks in murine blood leucocytes and bone marrow cells. The dose-dependent protection was more pronounced in bone marrow cells than in blood leucocytes. Administration of 175 mg/kg body weight of the drug (i.p.) 1 h prior or immediately after whole body irradiation of mice showed that the decrease in strand breaks depended on the post-irradiation interval at which the analysis was done. The observed time-dependent decrease in the DNA strand breaks could be attributed to enhanced DNA repair in troxerutin administered animals. Thus in addition to anti-erythrocytic, anti-thrombic, fibrinolytic and oedema-protective rheological activity, troxerutin offers protection against gamma-radiation-induced micronuclei formation and DNA strand breaks and enhances repair of radiation-induced DNA strand breaks.
研究了曲克芦丁对小鼠体内不同组织中γ射线诱导的DNA链断裂的影响,以及在体外人外周血淋巴细胞和体内小鼠血网织红细胞中微核的形成。用1 mM曲克芦丁处理可显著抑制人淋巴细胞中的微核诱导。在体外照射(2 Gy)条件下,曲克芦丁以浓度依赖性方式保护人外周血白细胞免受辐射诱导的DNA链断裂。在全身辐射暴露前后给小鼠腹腔注射曲克芦丁(175 mg/kg体重)可显著抑制血网织红细胞中的微核形成。在4 Gy γ射线照射前1 h给予不同剂量(75、125和175 mg/kg体重)的曲克芦丁,可使小鼠血白细胞和骨髓细胞中DNA链断裂的产量呈剂量依赖性降低。剂量依赖性保护在骨髓细胞中比在血白细胞中更明显。在小鼠全身照射前1 h或照射后立即腹腔注射175 mg/kg体重的药物表明,链断裂的减少取决于进行分析的照射后间隔时间。观察到的DNA链断裂随时间的减少可能归因于给予曲克芦丁的动物中DNA修复增强。因此,除了抗红细胞、抗血栓、纤维蛋白溶解和水肿保护的流变学活性外,曲克芦丁还能保护免受γ射线诱导的微核形成和DNA链断裂,并增强辐射诱导的DNA链断裂的修复。