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

Abstract

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.