Hassoun E A, Bagchi D, Stohs S J
School of Pharmacy and Allied Health Professions, Creighton University, Omaha, NE 68178, USA.
Toxicol Lett. 1995 Apr;76(3):245-50. doi: 10.1016/0378-4274(95)80009-3.
Pregnant CF1 mice were given 30 micrograms 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg or the vehicle as a single i.p. dose on day 12 of gestation and killed 48 h later. Increases in DNA elution rate constants (single strand breaks) in fetal and placental nuclei of 1.8- and 2.3-fold, respectively, were observed. Increases in lipid peroxidation (thiobarbituric acid reactive substances) in placental and fetal tissues of 1.9- and 1.5-fold, respectively, were also observed. TCDD administration produced increases in the amniotic fluid levels of the lipid metabolites malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT), and acetone (ACON) of 2.5-, 1.6-, 1.4-, and 1.6-fold, respectively relative to control animals. The results suggest that reactive oxygen species may participate in the teratogenic effects of TCDD.
妊娠CF1小鼠在妊娠第12天腹腔注射30微克2,3,7,8-四氯二苯并对二恶英（TCDD）/千克或溶剂，48小时后处死。观察到胎儿和胎盘细胞核中DNA洗脱速率常数（单链断裂）分别增加了1.8倍和2.3倍。还观察到胎盘和胎儿组织中脂质过氧化（硫代巴比妥酸反应性物质）分别增加了1.9倍和1.5倍。与对照动物相比，TCDD给药使羊水中脂质代谢产物丙二醛（MDA）、甲醛（FA）、乙醛（ACT）和丙酮（ACON）的水平分别增加了2.5倍、1.6倍、1.4倍和1.6倍。结果表明，活性氧可能参与了TCDD的致畸作用。
