Keen C L, Mark-Savage P, Lönnerdal B, Hurley L S
Drug Nutr Interact. 1983;2(1):17-34.
The teratogenicity of D-penicillamine (DP) (dimethyl cysteine) was studied using the Sprague-Dawley rat. D-Penicillamine was fed during pregnancy at a level of 0 (control), 0.17, 0.83, or 1.66% of the diet. The frequency of resorptions, and the frequency and severity of malformations, increased with increasing levels of the drug. Maternal and fetal tissue copper levels were significantly lower in the DP groups than in controls, with the levels decreasing in a dose-related manner. Maternal and fetal zinc levels were lower in the 1.6% DP group than in controls. Maternal liver iron concentration was higher in the drug-fed rats than in controls, increasing in a dose-related manner. Fetal iron concentration was not consistently affected by the drug. Maternal and fetal manganese, calcium, and magnesium concentrations were similar among all groups. These results suggest that the teratogenicity of D-penicillamine may be due in part to induction of copper deficiency and, at high dose levels, zinc deficiency, caused by its chelating properties.
使用斯普拉格-道利大鼠研究了D-青霉胺（DP，二甲基半胱氨酸）的致畸性。在孕期以占饮食0（对照）、0.17%、0.83%或1.66%的水平喂食D-青霉胺。吸收的频率以及畸形的频率和严重程度随药物水平的增加而增加。DP组的母体和胎儿组织铜水平显著低于对照组，且水平呈剂量相关下降。1.6%DP组的母体和胎儿锌水平低于对照组。喂食药物的大鼠母体肝脏铁浓度高于对照组，呈剂量相关增加。胎儿铁浓度未受到药物的一致影响。所有组之间母体和胎儿的锰、钙和镁浓度相似。这些结果表明，D-青霉胺的致畸性可能部分归因于其螯合特性导致的铜缺乏诱导，以及高剂量水平下的锌缺乏。
