Possible mechanisms for protective effect of Naringenin on sodium arsenic-induced-testicular toxicity.

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.