Graphene oxide is degraded by neutrophils and the degradation products are non-genotoxic

Nanoscale ◽  
2018 ◽  
Vol 10 (3) ◽  
pp. 1180-1188 ◽  
Author(s):  
Sourav P. Mukherjee ◽  
Anda R. Gliga ◽  
Beatrice Lazzaretto ◽  
Birgit Brandner ◽  
Matthew Fielden ◽  
...  

Graphene oxide (GO) undergoes neutrophil myeloperoxidase (MPO) dependent degradation and the degradation products are non-genotoxic for human lung cells.

Small ◽  
2020 ◽  
Vol 16 (21) ◽  
pp. 1907686 ◽  
Author(s):  
Sourav P. Mukherjee ◽  
Govind Gupta ◽  
Katharina Klöditz ◽  
Jun Wang ◽  
Artur Filipe Rodrigues ◽  
...  

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Sandeep Mittal ◽  
Veeresh Kumar ◽  
Nitesh Dhiman ◽  
Lalit Kumar Singh Chauhan ◽  
Renu Pasricha ◽  
...  

Abstract Graphene derivatives (GD) are currently being evaluated for technological and biomedical applications owing to their unique physico-chemical properties over other carbon allotrope such as carbon nanotubes (CNTs). But, the possible association of their properties with underlying in vitro effects have not fully examined. Here, we assessed the comparative interaction of three GD - graphene oxide (GO), thermally reduced GO (TRGO) and chemically reduced GO (CRGO), which significantly differ in their lateral size and functional groups density, with phenotypically different human lung cells; bronchial epithelial cells (BEAS-2B) and alveolar epithelial cells (A549). The cellular studies demonstrate that GD significantly ineternalize and induce oxidative stress mediated cytotoxicity in both cells. The toxicity intensity was in line with the reduced lateral size and increased functional groups revealed more toxicity potential of TRGO and GO respectively. Further, A549 cells showed more susceptibility than BEAS-2B which reflected cell type dependent differential cellular response. Molecular studies revealed that GD induced differential cell death mechanism which was efficiently prevented by their respective inhibitors. This is prior study to the best of our knowledge involving TRGO for its safety evaluation which provided invaluable information and new opportunities for GD based biomedical applications.


2004 ◽  
Vol 112 (15) ◽  
pp. 1488-1495 ◽  
Author(s):  
Melanie Doyle ◽  
Kenneth G. Sexton ◽  
Harvey Jeffries ◽  
Kevin Bridge ◽  
Ilona Jaspers

2021 ◽  
Author(s):  
Taisho Yamada ◽  
Seiichi Sato ◽  
Yuki Sotoyama ◽  
Yasuko Orba ◽  
Hirofumi Sawa ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 750
Author(s):  
Werner E. G. Müller ◽  
Meik Neufurth ◽  
Shunfeng Wang ◽  
Heinz C. Schröder ◽  
Xiaohong Wang

The anti-cancer antitumor antibiotic bleomycin(s) (BLM) induces athyminic sites in DNA after its activation, a process that results in strand splitting. Here, using A549 human lung cells or BEAS-2B cells lunc cells, we show that the cell toxicity of BLM can be suppressed by addition of inorganic polyphosphate (polyP), a physiological polymer that accumulates and is released from platelets. BLM at a concentration of 20 µg ml−1 causes a decrease in cell viability (by ~70%), accompanied by an increased DNA damage and chromatin expansion (by amazingly 6-fold). Importantly, the BLM-caused effects on cell growth and DNA integrity are substantially suppressed by polyP. In parallel, the enlargement of the nuclei/chromatin in BLM-treated cells (diameter, 20–25 µm) is normalized to ~12 µm after co-incubation of the cells with BLM and polyP. A sequential application of the drugs (BLM for 3 days, followed by an exposure to polyP) does not cause this normalization. During co-incubation of BLM with polyP the gene for the BLM hydrolase is upregulated. It is concluded that by upregulating this enzyme polyP prevents the toxic side effects of BLM. These data might also contribute to an application of BLM in COVID-19 patients, since polyP inhibits binding of SARS-CoV-2 to cellular ACE2.


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