Maternal zinc metabolism and changes of metallothionein-1 and zinc transporter-1 in fetal congenital heart diseases
10.3760/cma.j.issn.1674-635X.2019.01.004
- VernacularTitle:先天性心脏病患儿母体孕期锌代谢及其相关调节子金属硫蛋白-1和锌转运蛋白-1的变化研究
- Author:
Chenju JIANG
1
;
Xinru HONG
;
Chaobin LIU
;
Fengzhu CHEN
;
Xiaoyu HE
;
Yulan WANG
;
Qinghua SUN
Author Information
1. 350025福州,中国人民解放军联勤保障部队第九○○医院福建医科大学福总临床医学院厦门大学附属东方医院妇产科科技部国家环境影响早期个体发育国际科技合作基地
- Keywords:
Zinc deficiency;
Congenital heart disease;
Pregnancy;
Metallothionein-1;
Zinc transporter-1
- From:
Chinese Journal of Clinical Nutrition
2019;27(1):18-25
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate maternal zinc metabolism and the changes of zinc-related factors as metallothionein-1 (MT1) and zinc transporter-1 (ZnT1) in certain types of congenital heart diseases (CHD).Methods Fifteen infants with interventricular septal defect,12 infants with atrial septal defect and 7 infants with tetralogy of Fallot,together with their mothers were enrolled,and normal infants and their mothers were enrolled by a ratio of 1 ∶ 1 with the above three types of CHD diseases.General conditions of the mothers,along with their diets and zinc-containing drug supplementation during the pregnancy,were surveyed.Maternal blood zinc levels and serum alkaline phosphatase activities at gestation week 32 and delivery or induced abortion,and the protein and mRNA expressions of MT1 and ZnT1 in maternal serum and placental tissue at delivery or induced abortion were assayed.Results The general conditions were comparable between the CHD group and control group.The ratio of the mothers taking more zinc-rich food was significantly lower in the CHD group than in the control group.Circulating zinc levels in interventricular septal defect (73.55±5.79 μmol/L),atrial septal defect (72.66±5.82 μmol/L) and tetralogy of Fallot (68.72±6.72 μmol/L) groups were significantly lower than those in the control groups (82.77± 7.88,84.58 ± 7.55 and 85.66 ± 7.30 μmol/L) at delivery (P all ＜ 0.05).Similar change patterns were seen for serum alkaline phosphatase activities.The relative quantities of serum MT1 and ZnT1 proteins in interventricular septal defect (73.22±36.54 and 68.55± 27.82),atrial septal defect (64.29± 38.26 and 74.55 ± 29.67) and tetralogy of Fallot (67.88± 30.50 and 70.13±29.65) groups were significantly lower than those in their corresponding control groups (166.31±67.43and 97.67±30.22,182.56±71.40 and 111.65±32.70,and 173.81±62.36 and 108.27±28.52,P＜0.01 or P＜0.05).The relative quantities of placental MT1 and ZnT1 proteins and mRNA expressions in interventricular septal defect (protein quantities 0.438±0.096 and 0.384±0.061,mRNA expressions 1.23±0.82 and 0.96±0.39),atrial septal defect (0.427±0.093 and 0.377±0.059,1.17±0.70 and 0.85±0.40) and tetralogy of Fallot (0.414±0.111 and 0.336±0.066,1.31±0.97 and 0.90±0.38) groups were significantly lower than those in their corresponding control groups (protein quantities 0.565±0.083 and 0.541±0.090,mRNA expressions 2.78± 1.06 and 1.67±0.33;protein quantities 0.622±0.136 and 0.493±0.079,mRNA expressions 2.85±0.89 and 1.72±0.38;protein quantities 0.637±0.125 and 0.521±0.089,mRNA expressions 3.21 ± 0.99 and 1.61±0.29;P＜0.01 or P＜0.05).Conclusion Mothers with their fetus of certain types of CHD are found zinc deficiency,and down-regulation of MT1 and ZnT1 expressions in the serum and placenta may involve in the pathogenesis of CHD when maternal zinc deficiency.
