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.

随着纳米技术的无处不在，暴露于人造纳米颗粒（NPs）的可能性越来越高，这可能会给下一代带来新的健康问题。最近的数据表明，活性氧的产生可能在炭黑纳米颗粒（CBNPs）引起的氧化损伤中起着不可或缺的作用。但是，确切的分子机理尚未阐明。因此，氧化应激，炎症和细胞凋亡途径在卵内CBNPs诱导的神经元毒性中的作用阐明了鸡胚的暴露。在孵育的第3天，将无病原体的特定Sasso受精卵用4.8、9.5和14μgCBNPs /鸡蛋接种，并与媒介物对照一起接种。以浓度依赖性的方式，接种CBNPs会引起氧化应激，这可以通过增加脂质过氧化物并减少总的抗氧化能力和谷胱甘肽水平以及脑组织中的过氧化氢酶活性来确定。抗氧化剂基因的mRNA转录水平显示血红素加氧酶-1和超氧化物歧化酶-1上调，而谷胱甘肽S-转移酶-α显着下调。另外，促炎基因；核因子-κB1被上调，而干扰素-γ被下调。凋亡标记caspase-8，caspase-3也明显下调，细胞色素c和B细胞CLL /淋巴瘤2的浓度不同，而caspase-2仅在较高浓度时才上调。总的来说，这些结果表明，CBNPs暴露介导的自由基的过度产生，特别是在较高浓度下，在基因表达水平上促成炎症和随后的细胞凋亡，从而揭示了CBNPs与与氧化剂，炎症和凋亡相关的基因之间可能的分子关系。回应。