Exposure to lead in mice leading to DNA damage and oxidative damage
铅染毒导致小鼠DNA损伤与氧化损伤

To study the genotoxicity and oxidative damage induced by subacute lead exposure in mice, different doses of lead acetate (0,10,50,100,500 mg·kg-1 respectively) were administered by oral gavage every other day for four weeks. The DNA damage of peripheral blood lymphocytes wasexamined using comet assay, and the ROS level and MDA content in the liver were also detected. The results showed that the ROS level in mitochondriaincreased with the increase of lead doses and there was significant difference in 500 mg·kg-1 lead-treated group compared with control group. The MDA content, the tail length and tail moment at the dosages of 50, 100, 500 mg·kg-1 all significantly increased compared with that of the control, and thechange of MDA had the same manner with that of the tail length as well as the tail moment. Therefore, the primary mechanism of lead toxicity may be thatlead can induce the free radical generation, followed by lipid peroxidation and DNA damage.