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作者用30mW/cm~2的2450MHz微波全身照射小鼠S-180肉瘤模型48只,1h/d,共8d观察到S-180细胞超微结构损伤,血中超氧化物歧化酶(SOD)活力(11.0±1.2vs 15.1±1.1U/10~6RBC)明显下降(P<0.01)、脂质过氧化产物—内二醛(MDA)浓度(5.64±0.58vs 4.04±0.64mmol/L)显著升高(P<0.01);同时发现SOD抑制剂-二乙基二硫代氨基甲酸钠(DDC)能增强微波辐射对S-180细胞超微结构,血中SOD活力(7.8±1.3vs 11.0±1.2U/10~6 RBC,P<0.01)和MDA浓度(6.98±0.55vs 5.64±0.58 mmol/L,P<0.01)的影响;并且S-180细胞超微结构损伤的程度与SOD活力下降和MDA浓度升高的程度有关。因此,我们认为微波辐射损伤肿瘤细胞超微结构的机理涉及自由基、脂质过氧化。
The mice were irradiated whole body with 30mW/cm~2 2450MHz microwave 48-day S-180 sarcoma model for 1 h/d for 8 days. Ultrastructure damage of S-180 cells and superoxide dismutase (SOD) activity in blood were observed. 11.0±1.2vs 15.1±1.1U/10~6RBC) decreased significantly (P<0.01), lipid peroxidation product-MDA increased (5.64±0.58vs 4.04±0.64mmol/L). P<0.01); It was also found that SOD inhibitor-diethyldithiocarbamate (DDC) could enhance the ultrastructure of S-180 cells under microwave irradiation, and the SOD activity in blood was (7.8±1.3 vs. 11.0±1.2U/10. (6 RBC, P<0.01) and MDA concentrations (6.98±0.55 vs 5.64±0.58 mmol/L, P<0.01); and the degree of ultrastructure damage and SOD activity decreased and MDA concentration increased in S-180 cells. The degree is related. Therefore, we believe that the mechanism of microwave radiation damage the ultrastructure of tumor cells involves free radicals, lipid peroxidation.