铅染毒导致小鼠DNA损伤与氧化损伤

为了研究亚急性铅暴露对小鼠的遗传毒性及氧化损伤的诱导,将不同剂量的醋酸铅对小鼠隔日灌胃4周,用彗星实验检测其外周血淋巴细胞DNA损伤,并测定肝组织中活性氧自由基(ROS)的水平和脂质过氧化主要终产物丙二醛(MDA)的含量.结果显示,随染铅剂量的增加,小鼠肝线粒体中的ROS水平明显升高,染铅剂量为500 mg·kg-1组与对照组相比有显著性差异;肝MDA含量以及淋巴细胞尾长和尾相显著增加,染铅剂量为50、100、500 mg·kg-1组与对照组相比均有显著性差异;MDA与尾长和尾相的变化趋势一致.诱导产生自由基并导致脂质过氧化作用增强及DNA损伤是铅引起机体损伤的主要机制之一.

Exposure to lead in mice leading to DNA damage and oxidative damage

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.