Comparative mouse lung injury by nickel nanoparticles with differential surface modification

Area of Science:

• Nanotoxicology
• Materials Science

Background:

• Nickel nanoparticles (Nano-Ni) induce oxidative stress, lung inflammation, and pulmonary toxicity.
• Limited research exists on how Nano-Ni surface modification impacts in vivo lung injury, inflammation, and fibrosis.

Purpose of the Study:

• To investigate the effects of Nano-Ni surface modification on lung injury, inflammation, and fibrosis.
• To compare Nano-Ni with partially passivated Nano-Ni (Nano-Ni-P) and carbon-coated Nano-Ni (Nano-Ni-C).

Main Methods:

• Dose-response and time-response studies in mice exposed to Nano-Ni.
• Analysis of bronchoalveolar lavage fluid (BALF) for inflammatory markers (neutrophils, CXCL1/KC, LDH, total protein).
• Assessment of lung tissue for fibrosis (H&E, Trichrome staining, hydroxyproline), MMP-2/9 activity, lipid peroxidation (TBARS), and DNA damage (8-OHdG).

Main Results:

• Nano-Ni induced dose- and time-dependent acute lung inflammation and injury, peaking at day 3 and persisting long-term.
• Long-term Nano-Ni exposure led to significant interstitial fibrosis and oxidative stress.
• Carbon-coated Nano-Ni (Nano-Ni-C) exposure resulted in significantly milder acute and chronic lung inflammation and injury compared to Nano-Ni and Nano-Ni-P.

Conclusions:

• Short-term Nano-Ni exposure causes acute lung effects, while long-term exposure leads to chronic inflammation and fibrosis.
• Surface modification of Nano-Ni alleviates pulmonary toxicity.
• Carbon coating offers significant protection against Nano-Ni-induced lung inflammation and fibrosis.