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

Abstract

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.