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Protective effect of didymin against 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin-induced reproductive toxicity in male rats

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A Correction to this article was published on 11 November 2023

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Abstract

Purpose

2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most potent environmental toxicants, which causes oxidative stress and adversely affects the male reproductive system. The current study aimed to evaluate the ameliorative role of didymin (DDM) against TCDD-induced testicular toxicity.

Methods

Forty-eight male Sprague–Dawley rats were divided into four equal groups (n=12). (i) Control group, (ii) TCDD-induced group was provided with 10 μg/kg/day of TCDD, (iii) TCDD + DDM group received 10 μg/kg/day of TCDD and 2 mg/kg/day of DDM, and (iv) DDM-treated group was administered with 2 mg/kg/day of DDM. After 56 days of treatment, biochemical, steroidogenic, hormonal, spermatogenic, apoptotic, and histopathological parameters were estimated.

Results

TCDD affected the biochemical profile by reducing the activities of antioxidant enzymes, while increasing the levels of malondialdehyde (MDA) and reactive oxygen species (ROS). Furthermore, it decreased the expressions of steroidogenic enzymes, 3β-hydroxysteroid dehydrogenase (HSD), 17β-HSD, steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage enzyme (CYP11A1), and 17α-hydroxylase/17, 20-lyase (CYP17A1), as well as reduced the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and plasma testosterone. Besides, epididymal sperm count, viability, and motility were decreased, while sperm morphological anomalies were increased. Moreover, TCDD altered the apoptotic profile by up-regulating the expressions of Bax and caspase-3, while downregulated the Bcl-2 expression. Additionally, histopathological damages were prompted due to TCDD administration. However, DDM restored all the TCDD-induced damages owing to its antioxidant, anti-apoptotic, and androgenic potential.

Conclusion

Our data suggested that DDM might play its role as a therapeutic agent against TCDD-prompted testicular toxicity.

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Acknowledgements

The authors extend their appreciation to the researchers supporting project number (RSP2023R502), King Saud University, Riyadh Saudi Arabia for funding this project.

Funding

The authors were grateful to the King Saud University, Riyadh, Saudi Arabia, with researchers’ supporting project number (RSP2023R502), for funding this project. The funding body has no role in designing the study.

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Authors and Affiliations

Authors

Contributions

MUI, AT, and HN designed the study, conceived the study, and analyzed the results. MUI conceived an initial part of the study, performed the experiment, and helped in compiling the results. AT wrote the manuscript. MUI, AT, HA, SR, and TA helped in writing the results. MUI, AT, SR, TA, HA, and AA made a substantial contribution in the interpretation of data and revising the manuscript for intellectual content. All authors have read and approved the final manuscript. The authors declare that all data were generated in-house and that no paper mill was used.

Corresponding authors

Correspondence to Muhammad Umar Ijaz or Suhail Razak.

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Ethical approval

The study was approved by the Institutional Research Ethics Committee of University of Agriculture, Faisalabad (DGS No. 21897-900), which is in compliance with the European Union of Animal Care and Experimentation (CEE Council 86/609).

Competing interests

The authors declare no competing interests.

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The original online version of this article was revised due to a retrospective Open Access cancellation.

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Tahir, A., Ijaz, M.U., Naz, H. et al. Protective effect of didymin against 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin-induced reproductive toxicity in male rats. Naunyn-Schmiedeberg's Arch Pharmacol 397, 2203–2214 (2024). https://doi.org/10.1007/s00210-023-02763-4

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  • DOI: https://doi.org/10.1007/s00210-023-02763-4

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