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


DEMİR S., Alemdar N. T., YULUĞ E., KULABER A., Demir E. A., Erdogan N. S., ...More

Environmental Toxicology, 2026 (SCI-Expanded, Scopus) identifier identifier

  • Publication Type: Article / Article
  • Publication Date: 2026
  • Doi Number: 10.1002/tox.70076
  • Journal Name: Environmental Toxicology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, Chimica, Compendex, EMBASE, Environment Index, Geobase, Greenfile, MEDLINE
  • Keywords: acetamiprid, chrysin, endoplasmic reticulum stress, inflammation, Nrf2, oxidative stress, testicular toxicity
  • Karadeniz Technical University Affiliated: Yes

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.