Significant progress in research on the toxicity mechanism of graphene

Liu Sijin, the State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, has made significant progress in the study of graphene toxicity mechanisms. Related research results were published in the American Chemical Society magazine ACS Nano (ACS Nano, 2013, DOI: 10.1021/nn402330b).
The superior physicochemical properties of graphene make it potentially useful in many fields. However, the ensuing environmental and health risks are also receiving increasing attention. At present, the molecular mechanism of action of graphene on the biological effects of macrophages is not completely clear. Liu Sijin's research team found that graphene oxide (GO) induces programmed necrosis of cells through the Toll-like receptor (TLR-4) acting on the surface of macrophage membranes.

The researchers found that GO can induce autocrine of tumor necrosis factor (TNF-α) by activating the TLR4 receptor. TNF-α acts on the TNF-α receptor on the surface of its cell membrane, phosphorylating its downstream receptor-interacting proteins 1 (RIP1) and 3 (RIP3), further inducing programmed necrosis of cells. During this process, GO-induced reactive oxygen species (ROS) also promotes the process of cell necrosis. At the same time, GO can accumulate in large amounts in macrophages, which can trigger the collapse of the cytoskeleton and the inhibition of phagocytic ability. Rho-related kinase (ROCK) plays an important role in the dynamic balance of the skeleton. The effect of GO on the cytoskeleton is achieved by inhibiting the activity of the kinase. This work is important to reveal the mechanism of cell death induced by graphene oxide.

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