A concise review of carbon nanotube's toxicology.

Carbon nanotubes can be either single-walled or multi-walled, each of which is known to have a different electron arrangement and as a result have different properties. However, the shared unique properties of both types of carbon nanotubes (CNT) allow for their potential use in various biomedical devices and therapies. Some of the most common properties of these materials include the ability to absorb near-infra-red light and generate heat, the ability to deliver drugs in a cellular environment, their light weight, and chemical stability. These properties have encouraged scientists to further investigate CNTs as a tool for thermal treatment of cancer and drug delivery agents. Various promising data have so far been obtained about the usage of CNTs for cancer treatment; however, toxicity of pure CNTs represents a major challenge for clinical application. Various techniques both in vivo and in in vitro have been conducted by a number of different research groups to establish the factors which have a direct effect on CNT-mediated cytotoxicity. The main analysis techniques include using Alamar blue, MTT, and Trypan blue assays. Successful interpretation of these results is difficult because the CNTs can significantly disrupt the emission of the certain particles, which these assays detect. In contrast, in vivo studies allow for the measurement of toxicity and pathology caused by CNTs on an organismal level. Despite the drawbacks of in vitro studies, they have been invaluable in identifying important toxicity factors, such as size, shape, purity, and functionalisation, the latter of which can attenuate CNT toxicity.

Anthranilate fluorescence marks a calcium-propagated necrotic wave that promotes organismal death in C. elegans.

For cells the passage from life to death can involve a regulated, programmed transition. In contrast to cell death, the mechanisms of systemic collapse underlying organismal death remain poorly understood. Here we present evidence of a cascade of cell death involving the calpain-cathepsin necrosis pathway that can drive organismal death in Caenorhabditis elegans. We report that organismal death is accompanied by a burst of intense blue fluorescence, generated within intestinal cells by the necrotic cell death pathway. Such death fluorescence marks an anterior to posterior wave of intestinal cell death that is accompanied by cytosolic acidosis. This wave is propagated via the innexin INX-16, likely by calcium influx. Notably, inhibition of systemic necrosis can delay stress-induced death. We also identify the source of the blue fluorescence, initially present in intestinal lysosome-related organelles (gut granules), as anthranilic acid glucosyl esters--not, as previously surmised, the damage product lipofuscin. Anthranilic acid is derived from tryptophan by action of the kynurenine pathway. These findings reveal a central mechanism of organismal death in C. elegans that is related to necrotic propagation in mammals--e.g., in excitotoxicity and ischemia-induced neurodegeneration. Endogenous anthranilate fluorescence renders visible the spatio-temporal dynamics of C. elegans organismal death.