(527c) Assessment on the Treatment of Carbon Soot for Activated Carbon Applications: Oxidative Stress and Apoptosis Induced in Human Cell Lines

Authors: 
Zhen, X., National University of Singapore
Ng, W. C., National University of Singapore
Dong, P., National University of Singapore
Dai, Y., Shanghai Jiaotong University
Neoh, K. G., National University of Singapore
Wang, C. H., National University of Singapore

In Singapore, approximately 30 ton/day of carbon based solid waste is produced from petroleum chemical process. Solid waste like carbon soot is generally disposed to landfill sites or re-utilized as secondary raw materials. Carbon soot has gained much attention in its re-utilization due to its high content of carbon for possible processing as absorbent materials. However, carbon soot also contains hazardous components such as heavy metals arising from either sources or petroleum chemical process. These components may be toxic to human health and environment, and pose many restrictions in its re-utilization due to the potential toxicity. Therefore, it is important to examine the possible toxicity effects of carbon soot and its mechanism on human health.  In this study, we performed chemical and microbial leaching on carbon soot to remove hazardous components before further processing it as activated carbon.  Subsequently, three human cell lines i.e. HepG2, MRC-5 and MDA-MB-231 were used to investigate the cytotoxicity, oxidative stress and apoptosis induction by carbon soot. Carbon soot induced dose-dependent and time-dependent cytotoxicity in HepG2, MRC-5 and MDA-MB-231 cells as demonstrated by MTS and LDH assays. Meanwhile, the flow cytometry assay and fluorescence microscope results indicated that the carbon soot induced apoptosis of HepG2, MRC-5 and MDA-MB-231 cells increased with the increasing concentration of carbon soot. Carbon soot was also found to induce oxidative stress in HepG2, MRC-5 and MDA-MB-231 cells as demonstrated by generation of reactive oxygen species (ROS) and the alteration of antioxidant superoxide dismutase (SOD) and glutathione (GSH) compared to the unexposed control cells. Further, co-treatment with N-(mercaptopropionyl)-glycine (N-MPG), a type of ROS scavenger formulations, could inhibit cells apoptosis induced by carbon soot and increase the viability of cells. These results may provide an explanation for the potential mechanism in HepG2, MRC-5 and MDA-MB-231 cytotoxicity under the effect of carbon soot. We hope that these findings could help to understand, in a microscopic scale, the threat and risk of these wastes to human.