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<p>This study examined the acute respiratory toxicity of NiCl<sub>2</sub> in mice, focusing on oxidative stress, tissue damage, and trace element dysregulation. Forty male KM mice were allocated to a saline control group and three NiCl<sub>2</sub> exposure groups (20, 60, 115&#xa0;mg/kg; <i>n</i> = 10/group). Serum analysis assessed oxidative stress (MDA, GSH, SOD), liver (AST, ALT), kidney (Cr, BUN) function, and TP. Lung and tracheal tissues were examined for histopathological/ultrastructural pathological changes and apoptosis. Tissue levels of Ni, Zn, Cu, Fe, Ca, Mg, and Mn were measured using spectrophotometry. Results revealed dose-responsive elevations in serum AST, ALT, BUN, Cr, and MDA, accompanied by diminished GSH, TP, and T-SOD (<i>P</i> &lt; 0.05). Nickel exposure caused tracheal pseudostratified columnar epithelium detachment, alveolar structural wall thickening and widened septa, capillary congestion, mitochondrial swelling in alveolar type-II cells, and increased pulmonary apoptosis (<i>P</i> &lt; 0.05). Ni accumulated predominantly in the liver, lung, and kidney, with concurrent Zn upregulation and Cu/Fe depletion (<i>P</i> &lt; 0.05), while Ca, Mg, and Mn levels remained stable. These findings demonstrate that acute NiCl<sub>2</sub> inhalation induces oxidative stress, impairs liver/kidney function, and provokes pulmonary apoptosis and mitochondrial damage. Ni disrupted Cu/Zn/Fe homeostasis but exhibited negligible effects on Ca, Mg, or Mn metabolism.</p>

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Effect of NiCl2 Intake Through Respiratory Tract on Antioxidant Capacity, Lung, and Trace Element Content in Mice

  • 期刊论文

  • 发表日期：

    2025年5月17日

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  • Aifei Du,
  • Shaohua Feng,
  • Xuan Zhou,
  • Yiyin Li,
  • Shangqing Lu,
  • Bangyuan Wu

摘要

This study examined the acute respiratory toxicity of NiCl2 in mice, focusing on oxidative stress, tissue damage, and trace element dysregulation. Forty male KM mice were allocated to a saline control group and three NiCl2 exposure groups (20, 60, 115 mg/kg; n = 10/group). Serum analysis assessed oxidative stress (MDA, GSH, SOD), liver (AST, ALT), kidney (Cr, BUN) function, and TP. Lung and tracheal tissues were examined for histopathological/ultrastructural pathological changes and apoptosis. Tissue levels of Ni, Zn, Cu, Fe, Ca, Mg, and Mn were measured using spectrophotometry. Results revealed dose-responsive elevations in serum AST, ALT, BUN, Cr, and MDA, accompanied by diminished GSH, TP, and T-SOD (P < 0.05). Nickel exposure caused tracheal pseudostratified columnar epithelium detachment, alveolar structural wall thickening and widened septa, capillary congestion, mitochondrial swelling in alveolar type-II cells, and increased pulmonary apoptosis (P < 0.05). Ni accumulated predominantly in the liver, lung, and kidney, with concurrent Zn upregulation and Cu/Fe depletion (P < 0.05), while Ca, Mg, and Mn levels remained stable. These findings demonstrate that acute NiCl2 inhalation induces oxidative stress, impairs liver/kidney function, and provokes pulmonary apoptosis and mitochondrial damage. Ni disrupted Cu/Zn/Fe homeostasis but exhibited negligible effects on Ca, Mg, or Mn metabolism.