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首页> 外文期刊>Reproductive toxicology >Embryonic oxidative stress as a mechanism of teratogenesis with special emphasis on diabetic embryopathy.
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Embryonic oxidative stress as a mechanism of teratogenesis with special emphasis on diabetic embryopathy.

机译：胚胎氧化应激是致畸的一种机制，尤其着重于糖尿病性胚胎病。

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Reactive oxygen species (ROS) are involved in the etiology of numerous diseases including cardio-vascular diseases and diabetes mellitus. There is evidence that several teratogens affect the developing embryo by increasing its oxidative stress and, because of its relatively weak antioxidant defense, especially at the early stages of organogenesis, result in severe embryonic damage. This mechanism seems to operate in diabetes-induced embryonic damage as well as in the mechanism of teratogenicity caused by ionizing radiation, hypoxia, alcohol and cocaine use and cigarette smoking. We studied the role of oxidative stress in diabetic induced embryopathy, both in vivo and in vitro. Under diabetic condition there was a significant decrease in the activity of endogenous antioxidant enzymes and of vitamins C and E in the embryos and their yolk sacs. The lowest activity was observed in the malformed experimental embryos when compared to experimental embryos without anomalies. Similar results were obtained in the Cohen diabetic rats, where the diabetic prone (CDs) rats were unable to increase their antioxidant enzyme activity in spite of the diabetes. Studies performed by other investigators show similar results. Human and animal studies show that the main mechanism of fetal damage induced by high levels of ionizing irradiation, cocaine and alcohol abuse, hypoxia and cigarette smoking is also by increased embryonic oxidative stress. Similarly, several drugs exert their teratogenic activity via embryonic oxidative stress. Abnormal placentation may also cause enhanced placental oxidative stress, resulting in embryonic death, preeclampsia or congenital anomalies. Inability of the developing embryo to cope with that stress may result in embryonic death and/or congenital anomalies. Animal studies also show that a variety of antioxidants are effective in decreasing the damaging effects of heightened oxidative stress induced by teratogens. Effective antioxidants, which might also be of clinical use, include vitamins C and E, carotenoids, folic acid, as well as synthetic products. Appropriate clinical studies with antioxidants in pregnancies of high risk to develop oxidative stress are needed, since non-toxic antioxidants might prove an efficient and inexpensive way to reduce the rate of some serious and sometimes fatal congenital anomalies.
机译：活性氧（ROS）与许多疾病的病因有关，包括心血管疾病和糖尿病。有证据表明，几种致畸剂通过增加其氧化应激影响发育中的胚胎，并且由于其相对较弱的抗氧化防御能力，尤其是在器官发生的早期阶段，会导致严重的胚胎损伤。该机制似乎在糖尿病引起的胚胎损伤以及电离辐射，缺氧，饮酒和可卡因的使用以及吸烟引起的致畸性机制中起作用。我们研究了体内和体外氧化应激在糖尿病引起的胚胎病中的作用。在糖尿病条件下，胚胎及其卵黄囊内源性抗氧化酶以及维生素C和E的活性显着下降。与没有异常的实验胚胎相比，在畸形的实验胚胎中观察到最低的活性。在科恩（Cohen）糖尿病大鼠中也获得了类似的结果，其中尽管糖尿病，但糖尿病倾向（CDs）大鼠仍无法增加其抗氧化酶活性。其他研究人员进行的研究显示了相似的结果。人类和动物研究表明，高水平的电离辐射，可卡因和酒精滥用，低氧和吸烟引起的胎儿损伤的主要机制也是由于胚胎的氧化应激增加。同样，几种药物通过胚胎氧化应激发挥其致畸活性。胎盘异常也可能导致胎盘氧化应激增强，导致胚胎死亡，先兆子痫或先天性异常。发育中的胚胎无法应对这种压力可能会导致胚胎死亡和/或先天性异常。动物研究还表明，多种抗氧化剂可有效降低致畸剂引起的增加的氧化应激的破坏作用。有效的抗氧化剂，也可能具有临床用途，包括维生素C和E，类胡萝卜素，叶酸以及合成产品。由于无毒的抗氧化剂可能被证明是一种有效且廉价的方法，可以降低某些严重的，有时是致命的先天性异常的发生率，因此，需要在高风险妊娠中使用抗氧化剂进行适当的临床研究。

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