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Effect of NiCl2 Intake Through Respiratory Tract on Antioxidant Capacity, Lung, and Trace Element Content in Mice
Aifei Du1, Shaohua Feng1, Xuan Zhou1
1College of Life Science, China West Normal University, Nanchong, 637000, Sichuan, China.
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.
Insights
Acute nickel chloride (NiCl2) exposure in mice caused significant oxidative stress, liver and kidney dysfunction, and lung tissue damage. Nickel accumulation disrupted essential trace element balance, particularly affecting copper and iron homeostasis.
Area of Science:
- Toxicology
- Environmental Health
- Biochemistry
Background:
- Nickel compounds are industrial pollutants with known toxicity.
- Understanding the acute respiratory effects of nickel chloride (NiCl2) is crucial for occupational safety and public health.
- Trace element dysregulation is a key mechanism in heavy metal toxicity.
Purpose of the Study:
- To investigate the acute respiratory toxicity of NiCl2 in mice.
- To assess NiCl2-induced oxidative stress, tissue damage, and trace element imbalances.
- To examine the impact of NiCl2 on pulmonary apoptosis and mitochondrial function.
Main Methods:
- Male KM mice were exposed to saline (control) or varying doses of NiCl2 (20, 60, 115 mg/kg).
- Serum biochemical markers for oxidative stress, liver/kidney function, and total protein were analyzed.
- Histopathological and ultrastructural examinations of lung and tracheal tissues were performed, alongside apoptosis assays.
- Tissue elemental analysis (Ni, Zn, Cu, Fe, Ca, Mg, Mn) was conducted using spectrophotometry.
Main Results:
- NiCl2 exposure led to dose-dependent increases in serum markers of liver and kidney damage (AST, ALT, BUN, Cr) and oxidative stress (MDA), while decreasing antioxidants (GSH, T-SOD).
- Histopathology revealed tracheal epithelial detachment, alveolar wall thickening, capillary congestion, mitochondrial swelling in alveolar type-II cells, and increased pulmonary apoptosis.
- Nickel accumulated in the liver, lungs, and kidneys, causing significant upregulation of zinc and depletion of copper and iron, without affecting calcium, magnesium, or manganese levels.
Conclusions:
- Acute NiCl2 inhalation induces significant respiratory toxicity, characterized by oxidative stress, impaired organ function, and pulmonary cellular damage.
- Nickel exposure disrupts the homeostasis of essential trace elements (Cu, Zn, Fe), contributing to its toxic effects.
- The findings highlight the critical need for controlling nickel exposure in occupational and environmental settings.
