Evidence map›Paper›PMID 41837325›Full record

ArticleEnvironmental toxicology2026

Chrysin Mitigates Acetamiprid-Induced Testicular Injury in Mice via Suppression of Endoplasmic Reticulum Stress and Inflammation.

Selim Demir, Nihal Turkmen Alemdar, Esin Yulug, Ali Kulaber, Elif Ayazoglu Demir, Nadire Sevdenur Erdogan, Ahmet Mentese, Yuksel Aliyazicioglu

Abstract read
In one paragraph

Article in Environmental toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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

1 citing paper in PubMed.

  1. Article
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.

Selim DemirDepartment of Medical Biochemistry, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkiye.ORCID https://orcid.org/0000-0002-1863-6280
Nihal Turkmen AlemdarDepartment of Medical Services and Techniques, Vocational School of Health Services, Recep Tayyip Erdogan University, Rize, Turkiye.ORCID https://orcid.org/0000-0002-8913-8692
Esin YulugDepartment of Histology and Embryology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkiye.ORCID https://orcid.org/0000-0002-8857-9234
Ali KulaberDepartment of Histology and Embryology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkiye.ORCID https://orcid.org/0000-0003-0874-8825
Elif Ayazoglu DemirDepartment of Chemistry and Chemical Processing Technologies, Macka Vocational School, Karadeniz Technical University, Trabzon, Turkiye.ORCID https://orcid.org/0000-0001-7188-2176
Nadire Sevdenur ErdoganDepartment of Histology and Embryology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkiye.ORCID https://orcid.org/0009-0008-1191-3020
Ahmet MenteseDepartment of Medical Biochemistry, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkiye.ORCID https://orcid.org/0000-0003-2036-5317
Yuksel AliyaziciogluDepartment of Medical Biochemistry, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkiye.ORCID https://orcid.org/0000-0001-9474-4307

Funding

Karadeniz Teknik Üniversitesi TSA-2024-11112
6 · The paper itself

Abstract

Acetamiprid (ACP) is a neonicotinoid pesticide that is extensively utilized for the management of insect populations, but its toxic effects on the male reproductive system have become a source of concern. Chrysin (CHR) is a natural flavone found in many plants and bee products, including honey and propolis. The objective of this study was to evaluate the protective effect of CHR on ACP-induced testicular injury in male Balb/c mice. ACP (20 mg/kg) and CHR applications (10 and 20 mg/kg, respectively) were conducted via intragastric route for a period of 14 days. The administration of CHR treatments resulted in a substantial improvement in oxidative stress and inflammation levels, achieved by the elimination of ACP's inhibition of the Nrf2 pathway. CHR treatments significantly reversed the ACP-induced depletion in serum testosterone and inhibin B levels. Specifically, the treatment of CHR at a dose of 20 mg/kg resulted in a substantial improvement in degenerative testicular findings induced by ACP, as indicated by a significant reduction in TUNEL (+) cell count. Furthermore, the provision of CHR treatments resulted in the cessation of the decline in sperm count and viability that had been induced by ACP, whilst concomitantly leading to a substantial reduction in the number of spermatozoa that exhibited severe abnormalities. These results suggest that CHR may have a protective effect against ACP-induced testicular damage; however, the results require further corroboration through the implementation of more comprehensive studies.

Indexed as

Endoplasmic Reticulum StressFlavonoidsInsecticidesPyridinesTestisAnimalsInflammationMaleMiceMice, Inbred BALB CNeonicotinoidsOxidative StressacetamipridchrysinFlavonoidsInsecticidesNeonicotinoidsPyridinesacetamipridchrysinendoplasmic reticulum stressinflammationNrf2oxidative stresstesticular toxicity

Identifiers

PMID41837325
PMCPMC13656873

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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.