Abstract:
Carbon black nanoparticles (CBNPs) are extensively utilized across industrial sectors, including polymers, printing inks, biosensors, food additives, and green technologies. However, their widespread use raises concerns regarding potential human exposure and associated toxicological risks. Although pulmonary toxicity of CBNPs has been reported, limited information exists on their neurotoxic and genotoxic consequences post oral exposure. In the present study, Swiss albino male mice were orally administered with CBNPs at doses of 5, 10, and 20 mg/kg body weight daily for 30 days. They were evaluated for neurotoxicity by analyzing neurochemical parameters, including antioxidant enzymes viz., catalase, alkaline phosphatase, total ATPase, and total protein and neurotransmitter levels viz., gamma-aminobutyric acid and dopamine. Histopathological examination of brain regions was performed to assess cytoarchitectural changes, while genotoxic effects were determined using comet assay and chromosomal aberration analysis in bone marrow cells. Dose-dependent neurotoxic responses were elicited by oral exposure to these nanoparticles, evidenced by a marked decrease in neurotransmitter levels and significant alterations in enzymatic activity. Histopathological and genotoxic alterations substantiated the biochemical findings, revealing neuronal degeneration, Purkinje cell loss, tissue necrosis, and nanoparticle accumulation in brain regions, along with increased chromosomal aberrations and DNA fragmentation. The observed effects were associated with oxidative stress-mediated cellular damage, indicating compromised neuronal integrity. The findings demonstrated that prolonged oral exposure to CBNPs induced significant neurotoxicity and genotoxicity in mice, likely mediated through oxidative stress and cellular disruption. The importance of conducting rigorous toxicological evaluations of these nanoparticles for developing safer nanoparticle designs to mitigate potential health risks was highlighted in this study.
