ArticleVeterinary world2025
Aryl hydrocarbon receptor signaling in male fertility: Protective role of resveratrol and disruptive effects of CH223191 in adult male rats.
Article in Veterinary world, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Propolis as a potential modulator of aryl hydrocarbon receptor signaling in inflammation.European cytokine network · 2026Review
- Physiological interplay among obesity, male fertility, and aryl hydrocarbon receptor in human and mice: A mini review.Open veterinary journal · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aim: The aryl hydrocarbon receptor (AhR) plays a pivotal role in spermatogenesis through its regulatory functions in redox balance and gene expression. This study aimed to investigate the effects of resveratrol (RES), a polyphenolic AhR modulator, and CH223191, a selective AhR antagonist, on male reproductive function in rats by assessing sperm quality, oxidative stress, testicular histopathology, and Materials and Methods: Forty adult male rats were randomly divided into four groups: (i) Control, (ii) dimethyl sulfoxide (vehicle), (iii) RES (100 mg/kg i.p., twice weekly), and (iv) AhR¯ (CH223191, 10 mg/kg i.p., twice weekly), treated for 60 days. Post-treatment, sperm motility, survival, viability, and DNA fragmentation were evaluated. Total antioxidant capacity (TAC), malondialdehyde (MDA) levels, testicular histopathology, and Results: RES significantly enhanced sperm motility, survival, and viability, reduced DNA fragmentation, and increased TAC while decreasing MDA levels. Histologically, RES preserved normal testicular architecture. In contrast, AhR inhibition through CH223191 led to marked reductions in sperm quality, elevated oxidative stress, increased DNA fragmentation, and severe testicular degeneration. qPCR analysis revealed upregulation of AhR expression in the RES group (fold change: +23.1%) and significant downregulation in the AhR¯ group (fold change: -72.6%), indicating differential modulation of AhR signaling pathways. Conclusion: RES positively modulates AhR activity, safeguarding testicular structure and enhancing sperm quality through antioxidant and anti-apoptotic mechanisms. Conversely, AhR antagonism disrupts spermatogenesis, underscoring the receptor's essential role in male fertility. These findings suggest the therapeutic potential of AhR-targeting agents like RES in ameliorating male reproductive dysfunctions associated with oxidative stress and xenobiotic exposure.
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