Evidence map›Paper›PMID 41632441›Full record

ArticleForensic toxicology2026

Possible role of ribosome biogenesis in the recovery from transient hepatic damage caused by ethylene glycol in rats.

Kana Unuma, Toshihiko Aki, Nana Kobayashi, Shintaro Isa, Akihiro Tojo

Abstract read
In one paragraph

Article in Forensic 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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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Kana UnumaDepartment of Forensic Medicine Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (ST), 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.
Toshihiko AkiDepartment of Forensic Medicine Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (ST), 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan. aki.legm@tmd.ac.jp.ORCID 0000-0003-4410-6432
Nana KobayashiDepartment of Forensic Medicine Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (ST), 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.
Shintaro IsaDepartment of Forensic Medicine Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (ST), 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.
Akihiro TojoDepartment of Nephrology & Hypertension, Dokkyo Medical University, 880 kitakobayashi, mibu, Tochigi, Japan.

Funding

Ministry of Education, Culture, Sports, Science, and Technology 20H03955Ministry of Education, Culture, Sports, Science, and Technology 22K10606
6 · The paper itself

Abstract

purposeEthylene glycol (EG), a widely used industrial compound, has been implicated in accidental poisoning and homicide. Although the nephrotoxic mechanisms of EG are well characterized, its acute hepatotoxic potential remains underexplored. This study investigated histopathological and molecular alterations in the liver of rats following acute administration of EG. Possible dysfunction of an anti-oxidative pathway involving ferroptosis (glutathione peroxidase 4, Gpx4; solute carrier family 7 member 11, SLC7A11) is also examined.

methodsMale rats (8-week-old, male) were orally administered EG (8 g/kg) and euthanized at 2 and 5 days post-exposure by an administration of an overdose of anesthetic (40 mg/kg sodium pentobarbital). Serological analysis was performed to assess liver function. Liver tissues were evaluated by histology, transmission electron microscopy, and transcriptome analysis.

resultsSerological findings indicated transient liver damage at 2 days post-exposure, followed by recovery at 5 days. Transmission electron microscopy revealed glycogen accumulation, corroborated by periodic acid-Schiff and periodic acid-methenamine silver staining. Histological analysis revealed an increased number of nucleoli, correlating with upregulation of ribosomal genes on microarray analysis, particularly at 5 days post-exposure. In addition, significant decreases in Gpx4 and SLC7A11 expression were observed in rat livers treated with EG and Huh-7 human hepatoma cells, suggesting reduced cellular antioxidative capacity as a contributing factor to transient liver damage.

conclusionsThese findings reveal a pathway underlying EG-induced transient liver damage and suggest a possible mechanism of recovery, thereby providing new insights into EG poisoning.

Indexed as

Chemical and Drug Induced Liver InjuryEthylene GlycolLiverRibosomesAnimalsFerroptosisGlycogenMaleMicroscopy, Electron, TransmissionPhospholipid Hydroperoxide Glutathione PeroxidaseRatsRats, Sprague-DawleyEthylene Glycolglutathione peroxidase 4, ratGlycogenPhospholipid Hydroperoxide Glutathione PeroxidaseEthylene glycolGpx4LiverNucleolusRibosomeSLC7A11

Identifiers

PMID41632441
PMCPMC13303457

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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 OpenQuestion graph.