Takagi A, Sai K, Umemura T, Hasegawa R, Kurokawa Y
Division of Toxicology, National Institute of Hygienic Sciences, Tokyo.
Jpn J Cancer Res. 1990 Mar;81(3):213-5. doi: 10.1111/j.1349-7006.1990.tb02551.x.
8-Hydroxydeoxyguanosine (8-OH-dG) levels were examined in liver and kidney DNA after di(2-ethylhexyl)phthalate (DEHP), di(2-ethylhexyl)adipate (DEHA) and phthalic anhydride administration to male 6-week-old F-344 rats in the diet at concentrations of 1.2, 2.5 and 1.5%, respectively. Significant increases in 8-OH-dG levels were observed only in the liver (target organ of DEHP and DEHA carcinogenesis) DNA after 1 and 2 weeks of treatment with DEHP and DEHA, respectively. The results suggest the involvement of oxidative DNA damage in hepatocarcinogenesis by peroxisome proliferators.
在雄性6周龄F-344大鼠的饮食中分别以1.2%、2.5%和1.5%的浓度给予邻苯二甲酸二(2-乙基己基)酯(DEHP)、己二酸二(2-乙基己基)酯(DEHA)和邻苯二甲酸酐后,检测肝脏和肾脏DNA中的8-羟基脱氧鸟苷(8-OH-dG)水平。仅在分别用DEHP和DEHA处理1周和2周后,在肝脏(DEHP和DEHA致癌作用的靶器官)DNA中观察到8-OH-dG水平显著升高。结果表明氧化DNA损伤参与了过氧化物酶体增殖剂诱导的肝癌发生过程。