Evidence map›Paper›PMID 40598691›Full record

ArticleBMC pharmacology & toxicology2025

Methimazole-induced reproductive endocrine system disruption and hepatotoxicity: insights from a Trichogaster trichopterus animal model.

Mahdi Ahmadinia, Tahereh Naji, Homayoun Hosseinzadeh Sahafi

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Article in BMC pharmacology & toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Mahdi AhmadiniaLung Transplantation Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Tahereh NajiBasic Sciences Department, Faculty of Pharmacy and Pharmaceutical Sciences, Tehran Medical Sciences, Islamic Azad University, Shariati Avenue, Dorahi Yakhzhal, Yasaman Avenue, Tehran, 1941933111, Iran. dr_naji@iau.ir.
Homayoun Hosseinzadeh SahafiIranian Fisheries Science Research Institute, Agricultural Research, Education and Extension Organization, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMethimazole is commonly prescribed for managing hyperthyroidism, although concerns regarding its reproductive and hepatic adverse effects persist. This study aimed to evaluate the dose-dependent effects of methimazole on reproductive endocrine system function and hepatic integrity using an animal model.

methodsAdult female three-spot gourami (Trichogaster trichopterus) were administered intramuscular injections of methimazole at doses of 0.025, 0.05, and 0.1 mg/kg body weight every other day for 20 days. Gonadosomatic Index (GSI), Hepatosomatic Index (HSI), sex steroid hormones (17β-estradiol, testosterone, 17-hydroxyprogesterone), liver enzymes (GOT, GPT), and histological alterations in ovarian and hepatic histology were assessed.

resultsMethimazole significantly reduced GSI in a dose-dependent manner, with the lowest value (3.33%, P < 0.05) observed at the highest dose. Although HSI increased slightly, differences among groups were not significant. Dose-dependent declines were observed in sex steroid hormones, with the most pronounced reduction at 0.1 mg/kg (P < 0.05), indicating significant disruption in steroidogenesis and ovarian function. Liver enzymes activity GOT and GPT were significantly elevated at doses of 0.05 and 0.1 mg/kg (P < 0.05), reflecting hepatic stress and potential hepatotoxicity. Histological analyses demonstrated significant disruption in ovarian follicle maturation, with oocytes arrested at early growth stages at higher methimazole doses. Furthermore, structural liver damage including hepatocyte hypertrophy, inflammation, and necrosis was observed at the highest methimazole dose.

conclusionMethimazole induces notable reproductive and hepatic disturbances, highlighting the importance of monitoring endocrine and hepatic parameters during clinical methimazole therapy, especially in reproductive-age populations. These findings underscore the potential risks associated with methimazole treatment and suggest careful clinical monitoring to mitigate possible reproductive and hepatic adverse effects.

Indexed as

Antithyroid AgentsChemical and Drug Induced Liver InjuryEndocrine DisruptorsLiverMethimazoleAnimalsDose-Response Relationship, DrugFemaleGonadal Steroid HormonesOvaryReproductionAntithyroid AgentsEndocrine DisruptorsGonadal Steroid HormonesMethimazoleHepatic enzymesHepatotoxicityMethimazoleReproductive toxicitySteroid hormonesTrichogaster trichopterus

Identifiers

PMID40598691
PMCPMC12217290

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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.