Heavy metal and metalloid - induced reproductive toxicity

Heavy metals and metalloid exposure are among the most common factors responsible for reproductive toxicity in human beings. Several studies have indicated that numerous metals and metalloids can display severe adverse properties on the human reproductive system. Metals like lead, silver, cadmium, uranium, vanadium, and mercury and metalloids like arsenic have been known to induce reproductive toxicity. Moderate to minute quantities of lead may affect several reproductive parameters and even affect semen quality. The ecological and industrial exposures to the various heavy metals and metalloids have disastrous effects on the reproductive system ensuing in infertility. This work emphasizes the mechanism and pathophysiology of the aforementioned heavy metals and metalloids in reproductive toxicity. Additionally, this work aims to cover the classical protective mechanisms of zinc, melatonin, chelation therapy, and other trending methods to prevent heavy metal-induced reproductive toxicity.     

A systematic review and quantitative assessment of sleep-disordered breathing during pregnancy and perinatal outcomes

Purpose

Previous investigations have suggested a strong association between sleep-disordered breathing (SDB) during pregnancy and perinatal outcomes. However, the results of the following replication studies were not always concordant. Therefore, this meta-analysis was conducted to evaluate the more reliable estimate.

Methods

A systematic literature search was performed on PubMed, Springer Link, and EMBASE to identify all eligible studies published before August 2013. Summary odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated using fixed or random effects model.

Results

A total of 24 publications met the inclusion criteria and were included in this meta-analysis. Findings demonstrated that moderate-to-severe SDB during pregnancy was associated with gestational diabetes mellitus (OR?=?1.78; 95 % CI, 1.29 to 2.46), pregnancy-related hypertension (OR?=?2.38; 95 % CI, 1.63 to 3.47), preeclampsia (OR?=?2.19; 95 % CI, 1.71 to 2.80), preterm delivery (OR?=?1.98; 95 % CI, 1.59 to 2.48), low birth weight (OR?=?1.75; 95 % CI, 1.33 to 2.32), neonatal intensive care unit (NICU) admission (OR?=?2.43; 95 % CI, 1.61 to 3.68), intrauterine growth restriction (OR?=?1.44; 95 % CI, 1.22 to 1.71), and Apgar score of <7 at 1 min (OR?=?1.78; 95 % CI, 1.10 to 2.91) based on all studies but not gestational age and birth weight.

Conclusions

This meta-analysis revealed that moderate-to-severe SDB during pregnancy may be associated with most of adverse perinatal outcomes. Further well-designed studies are warranted to confirm our findings.     

Folic acid supplementation during pregnancy protects against lipopolysaccharide-induced neural tube defects in mice

Folic acid is a water-soluble B-complex vitamin. Increasing evidence demonstrates that physiological supply of folic acid during pregnancy prevents folic acid deficiency-related neural tube defects (NTDs). Previous studies showed that maternal lipopolysaccharide (LPS) exposure caused NTDs in rodents. The aim of this study was to investigate the effects of high-dose folic acid supplementation during pregnancy on LPS-induced NTDs. Pregnant mice were intraperitoneally injected with LPS (20 μg/kg/d) from gestational day (GD) 8 to GD12. As expected, a five-day LPS injection resulted in 19.96% of fetuses with NTDs. Interestingly, supplementation with folic acid (3 mg/kg/d) during pregnancy significantly alleviated LPS-induced NTDs. Additionally, folic acid significantly attenuated LPS-induced fetal growth restriction and skeletal malformations. Additional experiment showed that folic acid attenuated LPS-induced glutathione (GSH) depletion in maternal liver and placentas. Moreover, folic acid significantly attenuated LPS-induced expression of placental MyD88. Additionally, folic acid inhibited LPS-induced c-Jun NH2-terminal kinase (JNK) phosphorylation and nuclear factor kappa B (NF-κB) activation in placentas. Correspondingly, folic acid significantly attenuated LPS-induced tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in placentas, maternal serum and amniotic fluid. In conclusion, supplementation with high-dose folic acid during pregnancy protects against LPS-induced NTDs through its anti-inflammatory and anti-oxidative effects.     

妊娠期肝内胆汁淤积症对分娩结局影响的出生队列研究

目的 探讨孕中期和孕晚期妊娠期肝内胆汁淤积症(ICP)对分娩结局的影响。方法 在马鞍山市优生优育队列(MABC)中,将孕周≤14周、符合入组标准的孕妇共3 474人纳入队列,在首次产检时收集孕妇的一般人口学信息,并收集孕中期和孕晚期血清总胆汁酸(TBA)的检测结果,符合临床诊断的作为病例,采用logistic回归分析孕中期和孕晚期ICP对分娩结局的影响。结果 最终分析的样本人数为2 978人,ICP发生率为6.5%(n=196),其中孕中期和孕晚期ICP发生率分别为1.4%(n=43)和5.1%(n=153)。控制了潜在的混杂因素后,孕中期和孕晚期ICP均增加胎儿早产、低出生体重(LBW)、胎儿窘迫和羊水粪染的风险,OR值(95% CI)分别为6.42(2.59~15.93)和3.73(2.07~6.72);6.52(2.19~19.45)和4.90(2.43~9.90);2.91(1.27~6.67)和1.88(1.11~3.19);2.34(1.19~4.61)和1.66(1.11~2.48),并且孕中期ICP组发生上述不良分娩结局的风险远远高于孕晚期ICP组。结论 孕中期和孕晚期ICP均显著增加胎儿不良分娩结局的风险,孕中期ICP尤其值得关注,早期发现和干预对降低不良分娩结局的发生意义重大。     

青少年遭受同伴欺凌与抑郁症状关系的纵向交叉滞后分析

  目的  探讨青少年不同类型欺凌行为和抑郁症状之间的关系, 为进一步预防青少年同伴欺凌提供科学依据。  方法  基于2019年9月(T1)和2020年9月(T2)对安徽省淮北市1 687名青少年队列随访数据, 采用交叉滞后回归方法探讨不同类型同伴欺凌与抑郁症状的相互关系。  结果  T2时遭受欺凌行为(躯体欺凌、言语欺凌、关系欺凌、网络欺凌)和抑郁症状得分均低于T1时, 差异均有统计学意义(t值分别为13.60, 8.61, 7.24, 3.76, 8.29, P值均 < 0.01)。两个时期青少年的欺凌行为与抑郁症状之间均呈正相关(P值均 < 0.01);交叉滞后回归分析显示, T1时期的遭受躯体、言语、关系和网络欺凌均能正向预测T2时期的抑郁症状(β值分别为0.06, 0.04, 0.12, 0.05), T1时期的抑郁症状也能正向预测T2时期遭受躯体、言语、关系和网络欺凌(β值分别为0.07, 0.10, 0.13, 0.10)(P值均 < 0.05)。  结论  青少年同伴欺凌与抑郁症状之间相互影响, 存在一定的双向关联。     

Time-specific effect of prenatal stressful life events on gestational weight gain

Objective

To investigate the time-specific effect of maternal exposure to prenatal stressful life events (SLEs) on gestational weight gain (GWG) and to determine whether pre-pregnancy body mass index (BMI) modifies the effect.

Methods

Between March and November 2008, data were collected from 1800 pregnant women who received prenatal check-ups in Hefei, China, after 32 completed weeks of gestation. Participants completed a structured interview on demographic characteristics and a checklist of SLEs during different stages of pregnancy. GWG during pregnancy was determined by self-reported pre-pregnancy weight and measured weight at delivery.

Results

There was a significant dose–response relationship between prenatal SLEs in the first, but not the second or third, trimester and GWG. For each 1-unit increase in SLEs during the first trimester, there was a reduction in GWG of approximately 0.497 kg (95% confidence interval, 0.176–0.817 kg). After stratification by pre-pregnancy BMI, a significant negative association between SLEs in the first trimester and GWG was observed among women with pre-pregnancy normal (β = − 0.796; 95% CI, − 1.291 to − 0.301) and low (β = − 1.066; 95% CI, − 2.180 to − 0.048) weight.

Conclusion

The effect of prenatal SLEs on GWG depends on the timing of maternal exposure to stress and varies according to pre-pregnancy BMI.