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<p>Manganese, an essential trace element critical for maintaining normal physiological functions in living organisms, may exert adverse health effects under conditions of excessive exposure. The present study sought to investigate the impact of manganese exposure on mouse testicular tissue and elucidate the underlying mechanisms. Male ICR mice were administered graded doses of manganese chloride (MnCl₂) via oral gavage. The extent of testicular injury was assessed through histopathological examination, while oxidative stress levels were quantified using biochemical assay kits. The expression of key proteins and mRNA involved in the Nrf2 signaling pathway was evaluated by immunofluorescence, Western blotting, and real-time quantitative PCR. The results demonstrated that manganese exposure induced pathological damage in testicular tissue, triggered oxidative stress responses, and significantly reduced antioxidant capacity. Further mechanistic analysis revealed that manganese exposure downregulated the protein and mRNA expression levels of Nrf2, HO-1, and NQO-1, concurrently upregulated Keap1 expression, and suppressed Nrf2 nuclear translocation. In summary, manganese exposure can cause testicular tissue damage. This is associated with oxidative stress and inhibition of the Nrf2 signaling pathway.</p>

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Effects of Excessive Manganese Exposure on Testicular Oxidative Stress, Histopathology, and Nrf2 Signaling Pathway in Mice

  • 期刊论文

  • 发表日期：

    2026年5月12日

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  • Dianyi Peng,
  • Fuqing Feng,
  • Heng Yin,
  • Jianfei Zhao,
  • Shanchuan Cao,
  • Li Zhang,
  • Jingbo Liu

摘要

Manganese, an essential trace element critical for maintaining normal physiological functions in living organisms, may exert adverse health effects under conditions of excessive exposure. The present study sought to investigate the impact of manganese exposure on mouse testicular tissue and elucidate the underlying mechanisms. Male ICR mice were administered graded doses of manganese chloride (MnCl₂) via oral gavage. The extent of testicular injury was assessed through histopathological examination, while oxidative stress levels were quantified using biochemical assay kits. The expression of key proteins and mRNA involved in the Nrf2 signaling pathway was evaluated by immunofluorescence, Western blotting, and real-time quantitative PCR. The results demonstrated that manganese exposure induced pathological damage in testicular tissue, triggered oxidative stress responses, and significantly reduced antioxidant capacity. Further mechanistic analysis revealed that manganese exposure downregulated the protein and mRNA expression levels of Nrf2, HO-1, and NQO-1, concurrently upregulated Keap1 expression, and suppressed Nrf2 nuclear translocation. In summary, manganese exposure can cause testicular tissue damage. This is associated with oxidative stress and inhibition of the Nrf2 signaling pathway.