Carbon nanotubes (CNTs) consist of a family of carbon built nanoparticles, whose biological effects depend on their physical characteristics and other constitutive chemicals (impurities and functions attached). CNTs are considered the twenty first century material due to their unique physicochemical characteristics and applicability to industrial product. The use of these materials steadily increases worldwide and toxic outcomes need to be studied for each nanomaterial in depth to prevent adverse effects to humans and the environment. Entrance into the body is physical, and usually few nanoparticles enter the body; however, once there, they are persistent due to their limited metabolisms, so their removal is slow, and chronic cumulative health effects are studied. Oxidative stress is the main mechanism of toxicity but size, agglomeration, chirality as well as impurities and functionalization are some of the structural and chemical characteristic contributing to the CNTs toxicity outcomes. Among the many toxicity pathways, interference with cytoskeleton and fibrous mechanisms, cell signaling, membrane perturbations and the production of cytokines, chemokines and inflammation are some of the effects resulting from exposure to CNTs. The aim of this review is to offer an up-to-date scope of the effects of CNTs on biological systems with attention to mechanisms of toxicity.
Recent studies have demonstrated that carbon nanotubes (CNTs) induce platelet aggregation, endothelial dysfunction and vascular thrombosis. However, there is little information on the effects of CNTs on fibrinolysis. We investigated the role of pristine-commercial single-walled carbon nanotubes (SWCNTs) with <3% Co content in fibrinolysis and their contribution to the induction of pro-thrombotic processes in human vein endothelial cells (HUVEC). SWCNTs alone produced concentration-dependent oxidation, as measured by a dithiothreitol oxidation assay. Internalized SWCNTs were located in HUVEC treated with 25 μg/ml using transmission electron microscopy, whereas treatment with 50 μg/ml compromised cell viability, and oxidative stress increased significantly at 5 μg/ml. The study showed that in HUVEC treated with 25 μg SWCNT/ml, fibrinolysis-related gene expression and protein levels had increased by 3-12 h after treatment (serpine-1: 13-fold; PLAT: 11-fold and PLAU: 2-fold), but only the PAI-1 protein was increased (1.5-fold), whereas tissue and urokinase plasminogen activator proteins (tPA and uPA, respectively) tended to decrease. In summary, pristine SWCNTs treatment resulted in evident HUVEC damage caused by cell fiber contact, internalization, and oxidative stress due to contaminant metals. The generation of endothelial dysfunction, as shown by the altered expression of genes and proteins involved in fibrinolysis, suggest that SWCNTs display pro-thrombotic effects.
Patients with cancer undergoing chemotherapy are at risk of thrombocytopenia. The co-incidence of cancerassociated venous thromboembolism (VTE) and thrombocytopenia is a frequent complication in patients with cancer. Especially in certain tumour entities at high VTE risk, chemotherapeutic agents with myelosuppressive effects are part of the standard of care. The management of cancer-associated VTE in the setting of chemotherapy-induced thrombocytopenia is challenging, in the absence of evidence from high-quality studies. Thrombocytopenia is associated with both increased risk of recurrent VTE and risk of bleeding during anticoagulation. In this case-based concise review, we aimed at summarizing available literature and expert consensus guidance on the treatment of cancer-associated VTE in patients with chemotherapy-induced thrombocytopenia.
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