Protective Role of Chrysin against Mercury Chloride-Induced Testicular Damage via Oxidative Stress, Inflammation,...

The aim of this research was to examine the potential ameliorative effects of chrysin (CHR) against mercuric chloride (HgCl₂)-induced testicular damage in rats. For this purpose, rats were divided into four groups: Control, CHR, HgCl₂ and HgCl₂ + CHR. HgCl₂ was administered intraperitoneally at a dose of 1.23 mg/kg, and CHR was administered orally at a dose of 50 mg/kg for 7 days. Biochemical, molecular and immunohistochemical analyses were performed to determine the effect of treatment-mediated changes in the testicular tissue. Based on the results obtained in testicular tissue, administration of HgCl₂ was observed to lower antioxidant markers, elevate malondialdehyde (MDA) levels, and increase inflammatory marker expression in rat testicular tissue. It also led to reduced testosterone levels. Additionally, there was a decrease in the expression of antiapoptotic B-cell lymphoma 2 (Bcl-2) an apoptosis marker while the levels of Caspase-3 and Bcl-2-associated X protein (Bax) were found to be higher. The endoplasmic reticulum stress marker protein kinase R-like ER kinase (PERK) and the autophagy marker Beclin-1 showed strong immunoreactivity. Additionally, HgCl₂ + CHR treatment were found to significantly reduce oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and autophagy processes in testicular tissue. In conclusion, HgCl₂ administration to rats caused testicular tissue damage compared to the other groups, but CHR treatment alleviated this damage. Overall, this demonstrates the potential ameliorative mechanisms of CHR as a possible agent for HgCl₂-induced testicular damage.