Generation of reactive oxygen species contributes to the development of carbon black cytotoxicity to vascular cells

Carbon black, a particulate form of pure elemental carbon, is an industrial chemical with the high potential of occupational exposure. Although the relationship between exposure to particulate matters (PM) and cardiovascular diseases is well established, the cardiovascular risk of carbon black has not been characterised clearly. In this study, the cytotoxicity of carbon black to vascular smooth muscle and endothelial cells were examined to investigate the potential vascular toxicity of carbon black. Carbon black (with distinct particle size, N330 36 nm) and (primary size, 28 350 nm) were treated to A-10, rat N990 (250 aortic smooth muscle cells and human umbilical vein endothelial cell line), ECV304, and cell viability was assessed by lactate dehydrogenase (LDH) leakage assay. Treatment of carbon black N990 resulted in the significant reduction of viability in A-10 cells at 100 íg/mL, the highest concentration tested, while N330 failed to cause cell death. Cytotoxicity to ECV304 cells was induced only by N330 at higher concentration 200 íg/mL, suggesting that ECV304 cells were relatively resistant to carbon black. Treatment of 100 íg/mL N990 led to the elevation of reactive oxygen species (ROS) detected by dichlorodihydrofluorescein (DCF) in A-10 cells. Pre-treatment of antioxidants, N-acetylcysteine (NAC) and sulforaphane restored decreased viability of N990-treated A-10 cells, and N-acetylcysteine, but not sulforaphane, attenuated N990-induced ROS generation in A-10 cells. Taken together, present study shows that carbon black is cytotoxic to vascular cells, and the generation of reactive oxygen contributes to the development of cytotoxicity. ROS scavenging antioxidant could be a potential strategy to attenuate the toxicity induced by carbon black exposure.

Authors: Lee, Jong Gwan; Noh, Won Jun; Kim, Hwa; Lee, Moo-Yeol ;Full Source: Toxicological Research 2011, 27(3), 161-166 (English) ;