| 摘要: |
| 目的 探讨孕期补锌对母儿汞毒性的拮抗作用及其可能的作用机制。方法 根据母血汞值选取病例组（妊娠中、晚期母血汞≥5.8 μg/L）、治疗组（妊娠中期母血汞≥5.8 μg/L，从妊娠16周起，每日补充锌元素10.6 mg直至分娩）、对照组（妊娠中、晚期母血汞正常）孕妇各30例，观察3组孕妇汞、锌水平变化及妊娠结局；应用蛋白质印迹法分析3组胎盘组织凋亡相关蛋白Bcl-2、Bax表达水平，应用原位末端标记法检测3组胎盘组织凋亡细胞阳性率。结果 治疗组妊娠晚期母血汞水平[（3.42±0.52）μg/L]低于病例组[（6.16±0.32）μg/L，P<0.05]，同时也较妊娠中期[（6.15±0.26）μg/L]下降（P<0.05）；而血锌水平[（671.34±44.65）μg/L]则高于病例组[（483.25±62.20）μg/L，P<0.05]，同时也较妊娠中期[（480.73±60.64）μg/L]升高（P<0.05）。病例组早产、胎膜早破、小于胎龄儿的发生率均高于治疗组（P均<0.05）。病例组胎盘组织凋亡细胞阳性率[（35.20±4.96）%]高于治疗组[（13.47±2.43）%]和对照组[（13.27±2.21）%，P均<0.05]，促凋亡蛋白Bax的表达水平（3 110.38±136.09）也高于治疗组（2 015.76±177.63）和对照组（2 009.90±152.61，P均<0.05），而凋亡抑制蛋白Bcl-2的表达水平（2 055.97±280.82）则低于治疗组（5 187.93±247.89）和对照组（5 308.83±259.97，P均<0.05）。结论 孕期补锌可拮抗汞对母儿的毒性作用，其机制可能与锌同时上调Bcl-2表达及下调Bax表达从而抑制细胞凋亡有关。 |
| 关键词: 汞中毒 锌 妊娠结局 细胞凋亡 Bcl-2 Bax |
| DOI：10.3724/SP.J.1008.2014.00274 |
| 投稿时间：2013-10-19修订日期：2013-11-21 |
| 基金项目: |
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| Zinc supplementation during pregnancy against mercury toxicity |
| ZHU Hong1 2,YANG Zu-jing2,HUI Ning1*,LIU Jun-xia3 |
(1. Department of Obstetrics and Gynecology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China;
2. Department of Obstetrics and Gynecology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China;
3. MOE-Shanghai Key Laboratory of Children's Environmental Health, Shanghai 200092, China
*Corresponding author.) |
| Abstract: |
| Objective To investigate the protective effect of zinc supplementation during pregnancy against mercury toxicity to mothers and newborns and the possible mechanism. Methods According to the maternal blood mercury levels at middle and late pregnancy, 90 pregnant women were equally divided into a case group (blood mercury≥5.8 μg/L at middle and late pregnancy), a treatment group (blood mercury≥5.8 μg/L at middle pregnancy, daily supplementation of 10.6 mg zinc till delivery), and a control group (normal blood mercury level at middle and late pregnancy). The levels of maternal blood mercury and zinc, and pregnancy outcome were observed in the three groups. The expression of apoptosis-associated protein Bcl-2 and Bax in the placenta tissue was detected by Western blotting analysis, and the apoptosis rate of cells in placenta tissue was detected by TUNEL assay in each group. Results The maternal blood mercury level at late pregnancy in the treatment group ([3.42±0.52] μg/L) was significantly lower than that in the case group ([6.16±0.32] μg/L, P<0.05) and that at middle pregnancy ([6.15±0.26 ] μg/L, P<0.05) in the treatment group; the blood zinc level in the treatment group ([671.34±44.65] μg/L) was significantly higher than that in the case group ([483.25±62.20] μg/L, P<0.05) and that at middle pregnancy ([480.73±60.64] μg/L, P<0.05) in the treatment group. The incidence rates of premature labour, premature rupture of membranes (PROM), and small for gestational age (SGA) in the case group were significantly higher than those in the treatment group (P<0.05). The apoptosis rate of cells in the placenta of the case group ([35.20±4.96]%) was significantly higher than those of the treatment group ([13.47±2.43]%) and the control group ([13.27±2.21]%, P<0.05). The expression level of Bax protein in the placenta of the case group (3 110.38±136.09) was significantly higher than those in the treatment group (2 015.76±177.63) and the control group (2 009.90±152.61, P<0.05).The expression level of Bcl-2 protein in the placenta of the case group (2 055.97±280.82) was significantly lower than that in the treatment group (5 187.93±247.89) and the control group (5 308.83±259.97, P<0.05). Conclusion Zinc supplementation during pregnancy has protective effect against mercury toxicity to mothers and newborns, which might be associated with up-regulation of Bcl-2 protein and down-regulation of Bax protein and the subsequent inhibition of cell apoptosis. |
| Key words: mercury poisoning zinc pregnancy outcome apoptosis Bcl-2 Bax |
