Evidence map›Paper›PMID 39665241›Full record

ArticleBirth defects research2024

Melatonin Attenuates PFOS-Induced Reproductive Toxicity of Pregnant Mice due to Placental Damage Via Antioxidant, Anti-Aging and Anti-Inflammatory Pathways.

Jianqiu Han, Zhikai Lu, Yalei Qi, Tengfei Liu, Yongmei Li, Honghui Han, Chen Zhao, Xueyun Ma

Abstract read
In one paragraph

Article in Birth defects research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Preeclampsia as a Study Model for Aging: The Klotho Gene Paradigm.International journal of molecular sciences · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Jianqiu HanCollege of Ecological Technology and Engineering, Shanghai Institute of Technology, Shanghai, China.
Zhikai LuCollege of Ecological Technology and Engineering, Shanghai Institute of Technology, Shanghai, China.
Yalei QiSchool of Life Sciences, East China Normal University, Shanghai, China.
Tengfei LiuSchool of Life Sciences, East China Normal University, Shanghai, China.
Yongmei LiSchool of Life Sciences, East China Normal University, Shanghai, China.
Honghui HanSchool of Life Sciences, East China Normal University, Shanghai, China.ORCID 0000-0002-2478-2735
Chen ZhaoMolecular Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
Xueyun MaRenji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.ORCID 0000-0002-6207-5740

Funding

Research and Development Founder of ECNU 11300-544000-02731
6 · The paper itself

Abstract

backgroundPerfluorooctane sulfonate (PFOS), an industrially synthesized persistent organic pollutant (POP), is intricately intertwined with human production and daily life. It has been discovered that PFOS is related to an elevated incidence of birth defects in fetuses. In contrast, melatonin (MLT), a hormone secreted by the pineal gland, has been demonstrated to exert a protective effect on reproductive development.

methodsThis paper investigates the protective effect of MLT against PFOS-induced reproductive toxicity by simultaneously orally administering MLT to pregnant mice exposed to PFOS. The therapeutic effect was evaluated through the monitoring of pregnancy outcomes, histological changes in the placenta, apoptosis and proliferation of placental spongiotrophoblast, as well as the expression of antioxidant enzyme genes, anti-aging genes, anti-inflammatory genes and other relevant genes.

resultsThe results of the study demonstrated that MLT treatment reversed the adverse pregnancy outcomes caused by toxic PFOS, including a low number of implanted fetuses, low neonatal fetal weight, and an increased number of resorbed fetuses. MLT treatment decreased the levels of MDA, an oxidation product generated by PFOS in the placenta of pregnant mice, and increased the levels of the antioxidant enzyme SOD. Additionally, MLT was able to maintain the normalization of placental structure, reduce apoptosis and sustain the proliferation of placental spongiotrophoblast by upregulating the expression of antioxidant genes (Nrf2, CAT) and anti-aging gene (Klotho), anti-inflammatory gene (Hsd11b2), thereby counteracting the oxidative stress caused by PFOS in the placenta, moreover, it also reduced the expression of inflammatory genes (Pycard) in the placenta.

conclusionsThe findings firmly establish the effectiveness of MLT in mitigating the harmful impacts of tainted PFOS on reproductive development during pregnancy. This provides a novel therapeutic approach for addressing PFOS-induced birth defects in fetuses.

Indexed as

Alkanesulfonic AcidsAntioxidantsFluorocarbonsMelatoninPlacentaReproductionAnimalsAnti-Inflammatory AgentsApoptosisFemaleMiceOxidative StressPregnancyAlkanesulfonic AcidsAnti-Inflammatory AgentsAntioxidantsFluorocarbonsMelatoninperfluorooctane sulfonic acidmelatonin (MLT)perfluorooctane sulfonate (PFOS)placentapregnant micereproductive toxicity

Identifiers

PMID39665241
PMCPMC11635750

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.