Quinoa Seed Extract Mitigates Sunset Yellow-induced Testicular Toxicity in Rats: Impact of NF-κB and Fas/FasL Signaling Pathways

Elsayed, Manar Ali; Ibrahim, Basma A.; Abaza, Marwa Tawfeek; Ahmed, Alshymaa Othman Hammam; Tawfik, Rania Magdy

doi:10.21608/esctj.2025.382371.1090

Quinoa Seed Extract Mitigates Sunset Yellow-induced Testicular Toxicity in Rats: Impact of NF-κB and Fas/FasL Signaling Pathways

Document Type : Original Article

Authors

¹ Forensic Medicine and Clinical Toxicology Department, Faculty of Human Medicine, Zagazig University, Zagazig, Egypt

² Medical Biochemistry and Molecular Biology Department, Faculty of Human Medicine, Zagazig University, Zagazig, Egypt

³ Human Anatomy and Embryology Department, Faculty of Human Medicine, Zagazig University, Zagazig, Egypt

10.21608/esctj.2025.382371.1090

Abstract

Background: The widespread usage of sunset yellow as a food additive has sparked debates over its possible harm. There is inconsistent research on the toxic effects of food azo dyes on human health. Quinoa seed retain advantages that are linked to antioxidant besides anti-inflammatory properties. Aim of the work: To examine the possible protective properties of quinoa extract on testicular toxicity induced by sunset yellow by assessing molecular, immunohistochemical, and morphometric studies. Material and methods: Four groups (6 rats each) were randomly assigned; control, quinoa extract (QE), sunset yellow (SY), and QE+SY groups. Markers of testicular dysfunction, inflammation, oxidant/antioxidant status, apoptosis were assessed besides histopathological and morphometric analysis. Results: QE administration improved testicular function through downregulation of testis specific transporter1 (TST1) gene besides androgen receptor upregulation. QE improved reproductive hormone levels and restored testicular histopathology. Also, QE restored redox balance as evidenced by the alleviation of malondialdehyde and 8-hydroxy-2-deoxyguanosine, increased both the reduced glutathione and catalase activities. QE moderated nuclear factor-kappa B (NF-κB) and Fas/FasL/Caspase signaling pathway as indicated by downregulation of NF-κB, Fas, FasL, Caspase-8 plus Caspase-3. In addition, QE improved the inflammation and apoptosis‐associated markers supported by immunostaining data of CD68 and P53, respectively. Conclusion: This study provided novel insights elucidating the mitigative potential of quinoa against SY‐induced testicular oxidative damage, inflammation, and apoptosis mediated via Fas/FasL/Caspase pathway. Recommendation: Further studies are essential to validate these mechanisms in clinical and experimental studies. Encouraging quinoa consumption as a clue for infertility problems and testicular dysfunction.

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