Objective: To investigate the subchronic lung injury induced by nano nickel oxide( nano NiO) and its mechanism from the view of nitrative stress in rats.
Methods: A total of 40 adult male Wistar rats were randomly divided into 5 groups, control group( normal saline), 0. 015, 0. 06 and 0. 24 mg / kg nano NiO groups and 0. 24 mg / kg micro NiO group. Rats received intratracheally instilled nano NiO, micro NiO and normal saline twice a week for 6 weeks, respectively. All rats were sacrificed after the exposure to obtain lung tissues. HE staining was used to observe the lung pathological changes. The content of nitric oxide, and the activities of total nitric oxide synthase( TNOS) and inducible nitric oxide synthase( iNOS) in pulmonary tissue homogenate were measured by microplate reader. The levels of interleukin-2( IL-2), transforminggrowth factor-beta( TGF-β), interferon-gamma( IFN-γ) and 8-hydroxy-2'-deoxyguanosine( 8-OHd G) in serum were detected by enzyme-linked immunosorbent assay( ELISA).
Results: The results of lung histopathology showed that the widened alveolar speta, inflammatory infiltration and nanoparticles deposition increased with the increasing dosage of nano NiO. Compared to control group, the content of NO and the activities of TNOS and iNOS in 0. 24 mg / kg nano NiO group increased in lung homogenate( P < 0. 05). The levels of IL-2, TGF-β and IFN-γ in nano NiO 0. 06 and 0. 24 mg /kg group were higher than that of control group, and the level of 8-OHd G increased in nano NiO 0. 24 mg / kg group when compared to control group in serum( P < 0. 05). Compared to micro NiO group, the levels of NO and iNOS in lung homogenate, and the serum levels of IL-2 and 8-OHd G increased after exposed to 0. 24 mg / kg nano NiO in rats( P < 0. 05).
Conclusion: Nano NiO can lead to lung injury in rats which may be related with nitrative stress reaction based on pulmonary inflammation.
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