Thompson Jennifer, Bannigan John
School of Medicine and Medical Science, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Ireland.
Reprod Toxicol. 2008 Apr;25(3):304-15. doi: 10.1016/j.reprotox.2008.02.001. Epub 2008 Feb 19.
The heavy metal cadmium (Cd) is a pollutant associated with several modern industrial processes. Cd is absorbed in significant quantities from cigarette smoke, and is known to have numerous undesirable effects on health in both experimental animals and humans, targeting the kidneys, liver and vascular systems in particular. However, a wide spectrum of deleterious effects on the reproductive tissues and the developing embryo has also been described. In the testis, changes due to disruption of the blood-testis barrier and oxidative stress have been noted, with onset of widespread necrosis at higher dosage exposures. Incorporation of Cd into the chromatin of the developing gamete has also been demonstrated. Ovarian Cd concentration increases with age, and has been associated with failure of progression of oocyte development from primary to secondary stage, and failure to ovulate. A further mechanism by which ovulation could be rendered ineffective is by failure of pick-up of the oocyte by the tubal cilia due to suboptimal expansion of the oocyte-cumulus complex and mis-expression of cell adhesion molecules. Retardation of trophoblastic outgrowth and development, placental necrosis and suppression of steroid biosynthesis, and altered handling of nutrient metals by the placenta all contribute to implantation delay and possible early pregnancy loss. Cd has been shown to accumulate in embryos from the four-cell stage onwards, and higher dosage exposure inhibits progression to the blastocyst stage, and can cause degeneration and decompaction in blastocysts following formation, with apoptosis and breakdown in cell adhesion. Following implantation, exposure of experimental animals to oral or parenteral Cd causes a wide range of abnormalities in the embryo, depending on the stage of exposure and dose given. Craniofacial, neurological, cardiovascular, gastrointestinal, genitourinary, and limb anomalies have all been described in placentates, with axial abnormalities and defects in somite structure noted in fish and ventral body wall defect and vertebral malformation occurring in the chick. In this paper, we examine the mechanisms by which Cd can affect reproductive health, and consider the use of micronutrients in prevention of these problems.
重金属镉（Cd）是一种与多种现代工业生产过程相关的污染物。大量的镉可从香烟烟雾中被吸收，并且已知在实验动物和人类中对健康有许多不良影响，尤其针对肾脏、肝脏和血管系统。然而，也有关于镉对生殖组织和发育中的胚胎产生广泛有害影响的描述。在睾丸中，已注意到由于血睾屏障破坏和氧化应激导致的变化，在高剂量暴露时会出现广泛的坏死。镉也已被证明会掺入发育中配子的染色质中。卵巢中的镉浓度随年龄增加，并且与卵母细胞从初级阶段发育到次级阶段的进程失败以及排卵失败有关。另一种可能使排卵无效的机制是由于卵母细胞 - 卵丘复合体扩张不理想以及细胞粘附分子表达错误，导致输卵管纤毛无法拾取卵母细胞。滋养层细胞生长和发育迟缓、胎盘坏死以及类固醇生物合成受抑制，以及胎盘对营养金属的处理改变，都导致着床延迟和可能的早期妊娠丢失。已表明镉从四细胞阶段起就会在胚胎中积累，高剂量暴露会抑制胚胎发育到囊胚阶段，并可导致囊胚形成后发生退化和解聚，伴有细胞凋亡和细胞粘附破坏。植入后，实验动物经口或经肠外途径接触镉会导致胚胎出现广泛的异常，这取决于接触阶段和给予的剂量。在胎盘动物中已描述了颅面、神经、心血管、胃肠、泌尿生殖和肢体异常，在鱼类中注意到有轴异常和体节结构缺陷，在鸡中则出现腹侧体壁缺陷和脊柱畸形。在本文中，我们研究了镉影响生殖健康的机制，并考虑使用微量营养素来预防这些问题。
