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January 22, 2026Biological Trace Element Research0 citationsOpen Access

Protective Role of Chrysin against Mercury Chloride-Induced Testicular Damage via Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy Pathways

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SASerpil AygörmezMMMustafa MakavESEbru Karadağ Sarı

Key Points

  • This research aims to investigate how chrysin can protect against testicular damage caused by mercuric chloride in rats.
  • Rats were divided into four groups: Control, CHR, HgCl2, and HgCl2 + CHR.
  • HgCl2 was administered at a dose of 1.23 mg/kg intraperitoneally.
  • Chrysin was administered orally at a dose of 50 mg/kg for 7 days.
  • Biochemical, molecular, and immunohistochemical analyses were performed on testicular tissue.
  • HgCl2 treatment lowered antioxidant markers and increased malondialdehyde (MDA) levels in testicular tissue.
  • Testosterone levels were reduced, while apoptosis markers Caspase-3 and Bax showed increased expression.
  • Chrysin treatment significantly reduced oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress, and autophagy effects.

Abstract

Abstract The aim of this research was to examine the potential ameliorative effects of chrysin (CHR) against mercuric chloride (HgCl 2 )-induced testicular damage in rats. For this purpose, rats were divided into four groups: Control, CHR, HgCl 2 and HgCl 2 + CHR. HgCl 2 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 HgCl 2 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, HgCl 2 + CHR treatment were found to significantly reduce oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and autophagy processes in testicular tissue. In conclusion, HgCl 2 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 HgCl 2 -induced testicular damage.

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Cite This Study

Aygörmez et al. (2026) studied this question.

synapsesocial.com/papers/6971bd26642b1836717e1d65https://doi.org/10.1007/s12011-026-04993-y
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