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<p>Cadmium (Cd) is a toxic heavy metal found in the environment from natural (volcanic eruptions) and industrial sources, including mining, smelting, batteries, and fuel combustion. Studies have shown that oxidative stress, inflammation, and abnormal immune response are associated with Cd-induced hypothalamic-pituitary-testicular (HPT) toxicity. The dietary trace element zinc (Zn) prevents oxidative and inflammatory effects in diverse experimental models. The literature has reported that Zn inhibits Cd-mediated HPT toxicity. Our objective is to investigate the mechanisms by which Zn inhibits the Cd-induced HPT toxicity in rats. A 42-day waterborne exposure of Cd and Zn was administered to rats individually at 200&#xa0;μg/L or in a co-exposure. Treatment with Zn significantly (<i>p</i> &lt; 0.05) reduced inflammatory and oxidative imbalance, as well as indoleamine 2,3-dioxygenase (IDO) activity and expression in both the hypothalamus and testes of rats. Furthermore, a Zn-induced reduction (<i>p</i> &lt; 0.05) in cadmium (Cd) concentration led to fewer degenerating neurons in the hypothalamus and lower testicular injury scores observed in the Sertoli and Leydig cells on histological examination. Exposure to Zn also resulted in an increased (<i>p</i> &lt; 0.05) sperm count, motility, viability, and lowered morphological alterations due to its antagonistic effect on Cd-induced decrease in reproductive/pituitary hormones and steroidogenic enzyme activities. Zn displayed high binding affinity (−9.2&#xa0;kcal/mol) when docked with IDO, thus counteracting Cd-induced increase in IDO activity/expression by modulating redox imbalance.</p>

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Redox Perturbation in Cadmium-Mediated Hypothalamic, Pituitary, and Testicular Impairment and Protective Effects of Zinc in Rats Is Accompanied by Modulation of Tryptophan Catabolism Enzyme/Protein

  • 期刊论文

  • 发表日期：

    2026年1月25日

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  • Azubuike Peter Ebokaiwe,
  • Theresa Ezedom,
  • Uche Denis-Eboh,
  • Othuke Bensandy Odeghe,
  • Jacinta N. Obimma,
  • Olusanya Olasehinde

摘要

Cadmium (Cd) is a toxic heavy metal found in the environment from natural (volcanic eruptions) and industrial sources, including mining, smelting, batteries, and fuel combustion. Studies have shown that oxidative stress, inflammation, and abnormal immune response are associated with Cd-induced hypothalamic-pituitary-testicular (HPT) toxicity. The dietary trace element zinc (Zn) prevents oxidative and inflammatory effects in diverse experimental models. The literature has reported that Zn inhibits Cd-mediated HPT toxicity. Our objective is to investigate the mechanisms by which Zn inhibits the Cd-induced HPT toxicity in rats. A 42-day waterborne exposure of Cd and Zn was administered to rats individually at 200 μg/L or in a co-exposure. Treatment with Zn significantly (p < 0.05) reduced inflammatory and oxidative imbalance, as well as indoleamine 2,3-dioxygenase (IDO) activity and expression in both the hypothalamus and testes of rats. Furthermore, a Zn-induced reduction (p < 0.05) in cadmium (Cd) concentration led to fewer degenerating neurons in the hypothalamus and lower testicular injury scores observed in the Sertoli and Leydig cells on histological examination. Exposure to Zn also resulted in an increased (p < 0.05) sperm count, motility, viability, and lowered morphological alterations due to its antagonistic effect on Cd-induced decrease in reproductive/pituitary hormones and steroidogenic enzyme activities. Zn displayed high binding affinity (−9.2 kcal/mol) when docked with IDO, thus counteracting Cd-induced increase in IDO activity/expression by modulating redox imbalance.