Co-exposure of the organic nanomaterial fullerene C60 with benzo[a]pyrene in Danio rerio (zebrafish) hepatocytes: Evidence of toxicological interactions

RIBAS FERREIRA J.L.; LONNÉ, M.N.; FRANÇA, T.A.; MAXIMILLA, N.; LUGOKENSKI, T.H.; COSTA, P.G.; FILLMANN, G.; F.A. DE LA TORRE, F.R; MONSERRAT, J.M

AQUATIC TOXICOLOGY

ELSEVIER SCIENCE BV

Lugar: Amsterdam; Año: 2014

0166-445X

Compounds from the nanotechnology industry, such as carbon-based nanomaterials, are strong candi-dates to contaminate aquatic environments because their production and disposal have exponentiallygrown in a few years. Previous evidence shows that fullerene C60, a carbon nanomaterial, can facilitatethe intake of metals or PAHs both in vivo and in vitro, potentially amplifying the deleterious effects ofthese toxicants in organisms. The present work aimed to investigate the effects of fullerene C60in aDanio rerio (zebrafish) hepatocyte cell lineage exposed to benzo[a]pyrene (BaP) in terms of cell viability,oxidative stress parameters and BaP intracellular accumulation. Additionally, a computational dockingwas performed to investigate the interaction of the fullerene C60molecule with the detoxificatory andantioxidant enzyme GST. Fullerene C60provoked a significant (p < 0.05) loss in cellular viability whenco-exposed with BaP at 0.01, 0.1 and 1.0 g/L, and induced an increase (p < 0.05) in BaP accumulation inthe cells after 3 and 4 h of exposure. The levels of reactive oxygen species (ROS) in the cells exposed toBaP were diminished (p < 0.05) by the fullerene addition, and the increase of the GST activity observed inthe BaP-only treated cells was reduced to the basal levels by co-exposure to fullerene. However, despitethe potential of the fullerene molecule to inhibit GST activity, demonstrated by the computationaldocking, the nanomaterial did not significantly (p > 0.05) alter the enzyme activity when added to GSTpurified extracts from the zebrafish hepatocyte cells. These results show that fullerene C60can increasethe intake of BaP into the cells, decreasing cell viability and impairing the detoxificatory response byphase II enzymes, such as GST, and this latter effect should be occurring at the transcriptional level.