边高鹏1,2**,武有祯1,2,焦海华1
BIAN Gao-peng1,2**, WU You-zhen1,2, JIAO Hai-hua1
摘要: To explore the genotoxicity of isocarbophos to mice bone marrow cells and its mechanisms, Kunming mice were administered orally twice with isocarbophos at the doses of 0.11, 0.54, 1.08, 2.16 mg·kg-1, respectively, and the mice bone marrow cells were sampled after 30 h treatment. The DNA damage was assessed by the comet assay, and the ability to inhibit hydroxyl radical and superoxide anion radical was measured by Fenton reaction and xanthine oxidase method, respectively. Meanwhile, the relationships between the index of DNA fracture and the two inhibitory abilities abovementioned were also analyzed through regressive analysis. The results showed the tail moment and the Olive tail moment in all treatment groups were significantly higher than those in the control group (P<0.05). Furthermore, the two tail moments increased with the rise of the isocarbophos concentration in a dosedependent manner. The ability to inhibit superoxide anion radical was significantly induced (P<0.05) in the mice bone marrow at the dose of 0.11 mg·kg-1, but the ability to inhibit hydroxyl radical was poorly induced. However, the ability to inhibit both superoxide anion radical and hydroxyl radical was significantly induced (P<0.01) at the doses of 0.54, 1.08, 2.16 mg·kg-1. Both tail moment and Olive tail moment were significantly correlated with the increase of the activity to inhibit hydroxyl radical and superoxide anion radical, and displayed an obvious linear relationship (P<0.01). The results aforementioned suggested that isocarbophos had the stronger acute genotoxicity to mice bone marrow cells, and the mechanism of toxicological role in mice bone marrow cells may be DNA oxidative damages caused by isocarbophosinduced oxygen free radical.