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Updated: Sep 10, 2025
Preparation of Naringenin Solution for In Vivo Application
Published on: August 10, 2021
Possible mechanisms for protective effect of Naringenin on sodium arsenic-induced-testicular toxicity
Hana Sheykhi1, Fereshtesadat Fakhredini1, Mohammad Javad Khodayar2
1Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Background:
Sodium arsenite (SA), one of the compounds of arsenic, affects multiorgan systems including male reproduction. This study investigated whether Naringenin (NGN) could mitigate sodium SA-induced testicular toxicity by evaluating apoptosis, autophagy, and oxidative stress.
Methodes:
Male NMRI mice were given 40 mg/L SA in drinking water with or without intragastrically 50 mg/kg NGN for 35 days. Histology, serum testosterone concentration, Bax/Bcl-2 ratio, caspase-3 activity, and expression of autophagy-related biomarkers have been assessed. Malondialdehyde (MDA), glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) levels in testicular tissue were examined for the evaluation of oxidative stress.
Results:
SA caused histological damage and significantly increased Caspase-3 activity, the Bax/Bcl-2 ratio, while reducing testosterone concentration. Elevated MDA content and GSH, CAT, SOD levels indicate oxidative stress induced by SA in the mouse testicles (p < 0.05). The increased expression of Beclin-1 and ATG5, the elevated ratio of LC3-II/LC3- I proteins, and the diminished expression of the mTOR gene indicate autophagy induced by SA. NGN decreased the Bax/Bcl-2 ratio, and expression of Beclin-1, ATG5, LC3-II/ LC3-I ratio, while increasing mTOR gene expression. NGN could decrease oxidative stress and improve the histology and testosterone concentration in the SA-treated animals.
Conclusion:
NGN improves spermatogenesis by suppressing apoptosis, autophagy, and oxidative stress in SA-treated mice.
