Evidence mapPaperPMID 41908552Full record

ArticleFrontiers in toxicology2026

Integrated microbiome-metabolome analysis reveals multiorgan toxicity of 1-nitropyrene and the limited efficacy of ferroptosis inhibitor Fer-1 in rats.

Ning Yu, Shuguang Pang, Youmei Li, Hongcui Diao

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Article in Frontiers in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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

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3 · Its place in the literature

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No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Ning YuDepartment of Endocrinology, Jinan Central Hospital, Shandong University, Jinan, China.
Shuguang PangDepartment of Endocrinology, Jinan Central Hospital, Shandong University, Jinan, China.
Youmei LiDepartment of Endocrinology, Changqing District People's Hospital, Jinan, China.
Hongcui DiaoDepartment of Endocrinology, Jinan Central Hospital Affiliated to Shandong First Medical University, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: 1-Nitropyrene (1-NP), a prevalent nitro-polycyclic aromatic hydrocarbon, is increasingly recognized as a potential metabolic disruptor, yet its systemic biological effects remain insufficiently characterized. Methods: This study investigated the metabolic, immunological, hepatic, and microbiome alterations induced by chronic 1-NP exposure in rats and assessed whether ferroptosis inhibition via Fer-1 could mitigate these effects. Results: Although body weight was not significantly altered overall, high-dose exposure impaired growth from week 4. Exposed groups exhibited progressively elevated fasting blood glucose and impaired glucose tolerance, indicating significant disruption of glucose homeostasis. Serum biochemistry revealed dose-dependent reductions in HDL and total cholesterol, while histopathology confirmed hepatocyte ballooning, inflammation, and steatosis consistent with NAFLD-like progression. Hematological changes, including shifts in neutrophil and lymphocyte populations, suggested chronic inflammatory activation. Untargeted metabolomics identified extensive alterations in pathways related to glycolysis, tryptophan metabolism, glycerophospholipid metabolism, and ABC transporters. Gut microbiota analysis demonstrated reduced richness and significant compositional shifts, with functional predictions linking dysbiosis to xenobiotic degradation, lipid metabolism, and phosphotransferase systems. Integrated microbiome-metabolome analysis revealed coordinated disruptions in host-microbial metabolic networks. Fer-1 intervention modified specific metabolic and microbial signatures but did not substantially alleviate major toxic outcomes. Conclusion: Overall, chronic 1-NP exposure causes widespread metabolic injury driven by combined effects on host metabolism, immune regulation, hepatic function, and gut microbial ecology. These findings highlight 1-NP as a potent environmental metabolic disruptor and underscore the need for further mechanistic studies to inform mitigation strategies.

Indexed as

1-nitropyreneblood glucoseferroptosismetabolicnon-alcoholic fatty liver disease

Identifiers

PMID41908552
PMCPMC13021140

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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.