Carbon Black Nanoparticle Disruption of the Endocytic Pathway
Presentation Type
Poster
Presentation Type
Submission
Keywords
Carbon Black, nanoparticles, toxicity, autophagy, endocytosis, stress signaling
Department
Biology
Major
Biology, B.A. (Lauren) and Biology, B.S. (Siran)
Abstract
Carbon black (CB) is an environmental toxin and component of particulate matter created primarily from the incomplete combustion of petroleum products. This project investigates the impact of carbon black (CB) nanoparticle endocytosis on cell survival, with a focus on lysosomal integrity and stress signaling. We hypothesize that CB accumulation within cells disrupts the vesicular system in a dose-dependent manner, triggering pro-apoptotic stress signaling. Using three cultured mammalian cell lines, we observe a time-dependent increase in CB accumulation through an incorporation assay, confirming endocytic entry. WST-8 metabolic assays reveal a significant decline in cell viability at increasing CB concentrations. Preliminary immunofluorescence imaging suggests early signs of apoptosis, including nuclear condensation, while immunoblot analysis indicates disruption of the endolysosomal system, marked by elevated levels of the autophagy marker LC3-BII. Future assessments of the endocytic pathway will include assessing membrane integrity in endocytic vesicles and upregulation of stress signaling. This research highlights the cellular mechanisms underlying CB toxicity, with implications for understanding nanoparticle-induced environmental health risks.
Faculty Mentor
Dr. Jay Brewster
Funding Source or Research Program
Academic Year Undergraduate Research Initiative
Location
Waves Cafeteria
Start Date
11-4-2025 1:00 PM
End Date
11-4-2025 2:00 PM
Carbon Black Nanoparticle Disruption of the Endocytic Pathway
Waves Cafeteria
Carbon black (CB) is an environmental toxin and component of particulate matter created primarily from the incomplete combustion of petroleum products. This project investigates the impact of carbon black (CB) nanoparticle endocytosis on cell survival, with a focus on lysosomal integrity and stress signaling. We hypothesize that CB accumulation within cells disrupts the vesicular system in a dose-dependent manner, triggering pro-apoptotic stress signaling. Using three cultured mammalian cell lines, we observe a time-dependent increase in CB accumulation through an incorporation assay, confirming endocytic entry. WST-8 metabolic assays reveal a significant decline in cell viability at increasing CB concentrations. Preliminary immunofluorescence imaging suggests early signs of apoptosis, including nuclear condensation, while immunoblot analysis indicates disruption of the endolysosomal system, marked by elevated levels of the autophagy marker LC3-BII. Future assessments of the endocytic pathway will include assessing membrane integrity in endocytic vesicles and upregulation of stress signaling. This research highlights the cellular mechanisms underlying CB toxicity, with implications for understanding nanoparticle-induced environmental health risks.