Selenium reduces acrylamide‐induced testicular toxicity in rats by regulating HSD17B1, StAR, and CYP17A1 expression, oxidative stress, inflammation, apoptosis, autophagy, and DNA damage

Abstract

This study investigated the effects of Selenium (Se) on testis toxicity induced by Acrylamide (ACR) in rats. In our study, 50 male adult rats were used, and the rats were divided into five groups; control, ACR, Se0.5 + ACR, Se1 + ACR, and Se1. Se and ACR treatments were applied for 10 days. On the 11th day of the experimental study, intracardiac blood samples from the rats were taken under anesthesia and euthanized. Sperm motility and morphology were evaluated. Dihydrotestosterone, FSH, and LH levels in sera were analyzed with commercial ELISA kits. MDA, GSH, TNF‐α, IL‐6, and IL‐1β levels and SOD, GPx, and CAT, activities were measured to detect the level of oxidative stress and inflammation in rat testis tissues. Expression analysis of HSD17B1, StAR, CYP17A1, MAPk14, and P‐53 as target mRNA levels were performed with Real Time‐PCR System technology for each cDNA sample synthesized from rat testis RNA. Testicular tissues were evaluated by histopathological, immunohistochemical, and immunofluorescent examinations. Serum dihydrotestosterone and FSH levels decreased significantly in the ACR group compared to the control group, while LH levels increased and a high dose of Se prevented these changes caused by ACR. A high dose of Se prevented these changes caused by ACR. ACR‐induced testicular oxidative stress, inflammation, apoptosis, changes in the expression of reproductive enzymes, some changes in sperm motility and morphology, DNA, and tissue damage, and Se administration prevented these pathologies caused by ACR. As a result of this study, it was determined that Se prevents oxidative stress, inflammation, apoptosis, autophagy, and DNA damage in testicular toxicity induced by ACR in rats.

Protective effects of naringin on colistin‐induced damage in rat testicular tissue: Modulating the levels of Nrf‐2/HO‐1, AKT‐2/FOXO1A, Bax/Bcl2/Caspase‐3, and Beclin‐1/LC3A/LC3B signaling pathways

“…[66] Pro-inflammatory cytokines such as IL-1β cause acute responses of inflammation by inducing the expression of adhesion molecules in endothelial cells, stimulating inflammatory cells, and causing the proliferation of circulating leukocytes. [67] IL-1β generated by macrophages has a paracrine effect on Leydig cells. [68] IL-1β is also plays a role in apoptotic processes.…”

Associations of dietary selenium intake with the risk of chronic diseases and mortality in US adults

“…Several studies have shown that selenium deficiency increases the risk of metabolic disorders, such as dyslipidemia, abnormal glucose metabolism, and thyroid hormone dysfunction ( 21 ), through oxidative stress and abnormal activation of the PI3K/Akt signaling pathway ( 22 ). Moreover, Yildirim et al ( 23 ) showed that selenium can prevent oxidative stress-related damage in acrylamide-induced testicular toxicity in rats. In another study, Ibrahim et al ( 24 ) indicated that binaphthyl diselenide could significantly restore the defects of antioxidant defense mechanisms and exert anti-ulcer activity against ethanol-induced gastric injury.…”