Cosens G, Diamond I, Theriault L L, Hurley L S
Pediatr Res. 1977 Jun;11(6):758-64. doi: 10.1203/00006450-197706000-00013.
Magnesium-deficient fetuses exhibited malformations (44%), anemia, and edema. Maternal plasma magnesium levels at day 21 of pregnancy reflected the level of dietary magnesium (2.43 +/- 0.09 mg Mg/100 ml, control; 0.74 +/- 0.02 mg Mg/100 ml, deficient). Plasma magnesium levels of deficient fetuses showed similar decreases although all fetal magnesium values at term were hihger than maternal values from the same group (3.29 +/- 0.22 mg Mg/100 ml, control; 1.78 +/- 0.07 mg Mg/100 ml, deficient). Magnesium deficiency did not appear to affect the maternal blood parameters. However, when fetal blood was examined, all of the parameters measured were altered in magnesum-deficient fetuses (Table 2). No abnormalities in hemoglobin bands or plasma proteins were seen between any groups by electrophoresis. Measurement of total protein contents showed no differences between maternal blood protein contents, but total plasma protein from magnesium-deficient fetuses was significantly lower than controls (2.00 +/- 0.14 versus 2.62 +/- 0.13 g/100 ml), thus establishing a factor in fetal edema production. Morphologic data showed that in magnesium-deficient fetuses, fetal erythropoiesis was significantly greater in liver, adrenal glands, and spleen than in controls and that maturation was normoblastic. Stained and unstained peripheral blood smears of magnesium-deficient fetuses showed and obvious macrocytosis and at least 50% of the red cells stained abnormally, exhibiting pale areas. Erythrocytic morphology seen in fetal magnesium deficiency is consistent with inadequate filling of the cell by hemoglobin as suggested by Cohlan et al. (5), a probable cause of membrane collapse. The inadequate filling of magnesium-deficient red blood cells (RBC) with hemoglobin might be explained by a reduction in hemoglobin synthesis which is consistent with the reduced mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC) of the deficient fetal red cells. The role of magnesium in protein synthesis is also compatible with a reduction in hemoglobin synthesis, yet may not completely explain the abnormalities and resultant shortened lifespan of the red cells.
缺镁胎儿出现畸形（44%）、贫血和水肿。妊娠第21天母体血浆镁水平反映了膳食镁水平（对照组为2.43±0.09毫克镁/100毫升；缺镁组为0.74±0.02毫克镁/100毫升）。缺镁胎儿的血浆镁水平也有类似下降，尽管足月时所有胎儿的镁值均高于同组母体的值（对照组为3.29±0.22毫克镁/100毫升；缺镁组为1.78±0.07毫克镁/100毫升）。镁缺乏似乎未影响母体血液参数。然而，检查胎儿血液时，缺镁胎儿所有检测参数均发生改变（表2）。通过电泳，各实验组之间未发现血红蛋白条带或血浆蛋白异常。总蛋白含量测定显示母体血液蛋白含量无差异，但缺镁胎儿的血浆总蛋白显著低于对照组（2.00±0.14对2.62±0.13克/100毫升），这是导致胎儿水肿的一个因素。形态学数据显示，缺镁胎儿肝脏、肾上腺和脾脏的胎儿红细胞生成明显多于对照组，且成熟为正成红细胞性。缺镁胎儿的染色和未染色外周血涂片显示明显的大红细胞症，至少50%的红细胞染色异常，出现浅色区域。胎儿缺镁时的红细胞形态与Cohlan等人（5）提出的血红蛋白填充细胞不足一致，这可能是膜塌陷的原因。缺镁红细胞（RBC）血红蛋白填充不足可能是由于血红蛋白合成减少所致，这与缺镁胎儿红细胞平均血红蛋白（MCH）和MCH浓度（MCHC）降低一致。镁在蛋白质合成中的作用也与血红蛋白合成减少相符，但可能无法完全解释红细胞的异常及由此导致的寿命缩短。
