Fullerene (C60 and single- and multi-wall carbon nanotubes, SWCNT and MWCNT, respectively) is engineered to be redox active and it is thought that the potential toxicity of fullerene exposure is related to the formation of reactive oxygen species. During manufacture, transport or during scientific investigation, there is a potential for human or environmental exposure to nanoparticles. Several studies regarding human exposure have indicated reasons for concern. There is a lack of studies addressing the toxicity of engineered nanoparticles in aquatic species but one study using the fish, largemouth bass, exposed to fullerene has shown increased (10–17-fold) lipid peroxidation (LPO) in the brain. It is likely that repair enzymes or anti-oxidants may have been induced in gill and liver tissues that had reduced LPO compared to control tissues (Oberdörster, 2004). In support of that hypothesis, suppressive subtractive hybridization was used with liver tissue and the biotransformation enzyme, cytochrome P450, specifically CYP2K4, and other oxidoreductases related to metabolism, along with repair enzymes, were increased while proteins related to normal physiological homeostasis were decreased in fullerene-exposed fish. In a new study involving the exposure of a toxicological model fish species, the fathead minnow (Pimephales promelas) to water-soluble fullerene (nC60), uptake and distribution indicated that nC60 elevated LPO in the brain and induced expression of CYP2 family isozymes in the liver. In an in vitro study, BSA-coated SWCNT interfered with biotransformation enzyme activity. These studies taken together provide support to the hypothesis that the toxicity of manufactured nanoparticles is related to oxidative stress and provide insight into possible mechanisms of toxicity as well as providing information for evaluating the risk to aquatic organisms exposed to manufactured nanoparticles. © 2005 American Institute of Physics [ABSTRACT FROM AUTHOR]