In-ovo exposed carbon black nanoparticles altered mRNA gene transcripts of antioxidants, proinflammatory and apoptotic pathways in the brain of chicken embryo.

With ubiquitous applications of nanotechnology, there are increasing probabilities of exposure to manufactured nanoparticles (NPs), which might be posing emerging health concerns on the next generation. Recent data suggest that generation of reactive oxygen species may play an integral role in the carbon black nanoparticles (CBNPs)-induced oxidative injury; however, the exact molecular mechanism has not been clarified. Hence, the role of oxidative stress, inflammation and apoptosis pathways in the CBNPs-induced neuronal toxicity following in-ovo exposure of chicken embryo was elucidated. Specific pathogen-free fertilized Sasso eggs were inoculated with 4.8, 9.5 and 14 μg CBNPs/egg at the 3rd day of incubation alongside vehicle controls. In a concentration-dependent manner, CBNPs inoculation induced oxidative stress, which was ascertained by enhancement of lipid peroxides and diminishing total antioxidant capacity and glutathione levels, and catalase activity in brain tissues. mRNA transcript levels of antioxidant genes showed up-regulation of heme oxygenase-1 and superoxide dismutase-1, with marked down-regulation of glutathione S-transferase-α. Additionally, the pro-inflammatory genes; nuclear factor-κB1 was up-regulated, while interferon-γ was down-regulated. There is also a clear down-regulation in apoptotic markers caspase-8, caspase-3, cytochrome c and B-cell CLL/lymphoma 2 at the different concentrations, while caspase-2 is up-regulated only at higher concentration. Collectively, these results show that CBNPs exposure-mediated overproduction of the free radicals, particularly at higher concentration contributes to inflammation and subsequent cellular apoptosis at the gene expression level, thus unveiling possible molecular relationship between CBNPs and genes linked to the oxidant, inflammatory and apoptotic responses.