Paniagua-Castro Norma, Escalona-Cardoso Gerardo, Madrigal-Bujaidar Eduardo, Martínez-Galero Elizdath, Chamorro-Cevallos Germán
Department of Physiology, National School of Biological Sciences, National Polytechnic Institute, Prolongación Carpio y Plan de Ayala s/n, Colonia Santo Tomás, 11340 México D.F., Mexico.
Toxicol In Vitro. 2008 Feb;22(1):75-9. doi: 10.1016/j.tiv.2007.08.005. Epub 2007 Aug 23.
Cadmium (Cd) has an embryotoxic effect on laboratory animals expressed by growth retardation and induced craniofacial and skeletal malformations. Some of the mechanisms suggested to account for this reproduction damage include oxidative stress and lipoperoxidation. It has been shown that due to its antioxidant activity, glycine protects embryos from in vivo cadmium-induced teratogenicity. However, it is not known whether such protection may also be found in embryo cultures and what its possible mechanism of action might be. The purpose of this study was to determine whether the effect of glycine (1 mM) against the damage of CdCl(2) (1 microM) on the embryo, was direct or indirect. The amino acid was found to have significantly counteracted the effects of Cd by reducing the growth retardation and preventing the opening of the neural tube. Such protective effect seems to be partly due to decreased lipoperoxidation levels in embryos exposed to the metal, which would make it a direct effect.
镉（Cd）对实验动物具有胚胎毒性作用，表现为生长迟缓以及诱发颅面和骨骼畸形。一些被认为可解释这种生殖损伤的机制包括氧化应激和脂质过氧化。研究表明，由于其抗氧化活性，甘氨酸可保护胚胎免受体内镉诱导的致畸作用。然而，尚不清楚在胚胎培养中是否也能发现这种保护作用以及其可能的作用机制是什么。本研究的目的是确定甘氨酸（1 mM）对氯化镉（1 microM）对胚胎损伤的作用是直接的还是间接的。结果发现，该氨基酸通过减轻生长迟缓并防止神经管开放，显著抵消了镉的影响。这种保护作用似乎部分归因于暴露于该金属的胚胎中脂质过氧化水平的降低，这表明它是一种直接作用。
