Biochemistry Department Faculty of Medicine, Al-Quds University, Box 19356, East Jerusalem, Palestine.
Neurotoxicol Teratol. 2012 Jan-Feb;34(1):56-62. doi: 10.1016/j.ntt.2011.10.001. Epub 2011 Oct 13.
Phthalates are industrial chemicals widely used in consumer products, plastics and children toys, and the risk of exposure to phthalates, especially prenatal exposure, is a growing concern justifying the development of an animal model to better understand their effect. The present study was designed to evaluate the suitability of a chick model for phthalate DEHP teratogenicity and neurobehavioral teratogenicity, a model which is simple and devoid of potential confounding factors such as maternal toxicity, maternal-fetal unit and maternal-neonatal interactions; major findings were confirmed in the DBP study. Prehatch exposure to DEHP in doses ranging from 20 to 100 mg/kg, reduced the percent hatching from 80% in control eggs to 65%, and increased late hatchings from 12.5% in control eggs to 29.4%. In addition it induced developmental defects characterized by an opening or weakening of abdominal muscles allowing internal organs to protrude externally with or without a sac, omphalocele or gastroschisis, respectively. The effect was dose dependent ranging from 8% with DEHP (20 mg/kg) to 22% (100 mg/kg). Similar treatment with DBP 100mg/kg has reduced percentage hatching to 57% and increased late hatching to 37.5%, with a 14% increase in gastroschisis. Biochemical evaluation revealed elevated levels of alkaline phosphatase, which reflects non-specific toxicity of DEHP at such a high dose. Behavioral evaluation using an imprinting test and locomotor activity on chicks pretreated with DEHP (100 mg/kg) has shown an abolishment of imprinting performance from the control (0.65) preference ratio. DNA damage measurements of the metabolite 8-hydroxydeoxyguanosine (8-OH-dG) in blood samples showed an increase of 39.7% after prehatch exposure to phthalates. This was statistically significant for DEHP and indicates genetic toxicity, since part of the teratogenic activity is associated with oxidative stress and DNA damage.
邻苯二甲酸酯是一种广泛应用于消费品、塑料和儿童玩具的工业化学品,接触邻苯二甲酸酯(尤其是产前接触)的风险日益引起关注,这促使人们开发动物模型以更好地了解其影响。本研究旨在评估小鸡模型在邻苯二甲酸二(2-乙基己基)酯(DEHP)致畸性和神经行为致畸性方面的适用性,该模型简单且不存在母体毒性、母婴单位和母婴-新生儿相互作用等潜在混杂因素;主要发现已在邻苯二甲酸二丁酯(DBP)研究中得到证实。在孵化前,以 20 至 100mg/kg 的剂量接触 DEHP,会将对照卵中的孵化率从 80%降低至 65%,并将晚期孵化率从对照卵中的 12.5%增加至 29.4%。此外,它还会引起发育缺陷,表现为腹部肌肉张开或减弱,使内部器官向外突出,有或无囊、脐疝或腹裂。这种作用呈剂量依赖性,范围从 DEHP(20mg/kg)的 8%到 100mg/kg 的 22%。以 100mg/kg 的剂量用 DBP 处理,孵化率降至 57%,晚期孵化率增加至 37.5%,腹裂增加 14%。生化评估显示碱性磷酸酶水平升高,这反映了 DEHP 在如此高剂量下的非特异性毒性。用 DEHP(100mg/kg)预处理小鸡,然后进行印记测试和运动活动评估,结果显示印记性能从对照(0.65)偏好比完全丧失。对孵化前接触邻苯二甲酸酯的血液样本中代谢物 8-羟基脱氧鸟苷(8-OH-dG)的 DNA 损伤测量显示,其水平增加了 39.7%。这在统计学上对于 DEHP 是显著的,表明其具有遗传毒性,因为部分致畸活性与氧化应激和 DNA 损伤有关。