Graphene oxide (GO) has shown tremendous application potential as a biomedical material. However, its interactions with blood components are not yet well understood. In this work, we assess the toxicity of pristine GO (p-GO) and functionalized GO (GO-COOH and GO-PEI) to primary human peripheral blood T lymphocytes and human serum albumin (HSA), and also study the underlying toxic mechanism. Our results indicate that p-GO and GO-COOH have good biocompatibility to T lymphocytes at the concentration below 25 μg mL–1, but notable cytotoxicity above 50 μg mL–1. By contrast, GO-PEI exhibits significant toxicity even at 1.6 μg mL–1. Further investigations show that although p-GO does not enter into the cell or damage the membrane, its presence leads to the increase in reactive oxygen species (ROS), moderate DNA damage, and T lymphocyte apoptosis. Interestingly, little effect on T lymphocyte immune response suppression is observed in this process despite p-GO inflicting cell apoptosis. The toxic mechanism is that...

In Vitro Hemocompatibility and Toxic Mechanism of Graphene Oxide on Human Peripheral Blood T Lymphocytes and Serum Albumin

Biochemical characterization of the cholesterol-dependent growth of the NS-1 mouse myeloma cell line.

Sterol depletion reduces receptor-mediated low-density lipoprotein binding in NS-1 mouse myeloma cells☆

/pdf/drug-delivery-entry-and-intracellular-trafficking-of-23t12ntuog.pdf

Drug delivery, entry and intracellular trafficking of polymeric nanoparticles

Suppression of endocytosis in polyclonally activated Con A-stimulated T lymphocytes by 25-hydroxycholesterol.

Endocytosis in cytotoxic T-lymphocytes.

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Suppression of endocytosis in polyclonally activated Con A-stimulated T lymphocytes by 25-hydroxycholesterol.

Endocytosis in cytotoxic T-lymphocytes.