Toxicity Preventive Potential of Anti-Inflammatory CeO2 Nanoparticles in HUVE Cells

 The mechanism behind cerium oxide nanoparticles’ (CeO2 NPs) cytoprotective capability against cytotoxic nitric oxide (NO) donors and H2O2 is currently unknown. The lipopolysaccharide (LPS)-induced cytokines IL-1 and TNF- were dramatically reduced by CeO2 NPs that had been synthesised and described. Because NP-induced ROS/NO did not cause toxicity in HUVE cells, the main goal of this investigation was to determine the capacities of CeO2 NPs in terms of signalling effects that could have happened owing to reactive oxygen species (ROS) and/or NO. Two NO-donors were used in conjunction with CeO2 NPs in human umbilical vein-derived endothelial (HUVE) cells to achieve this goal. To our knowledge, there has been little investigation on CeO2 NPs’ modulatory ability against known NO-donors. SNP (sodium nitroprusside, #ab145732 from Abcam plc, Cambridge, UK) and DETA-NO (Z)-1-[N-(2-Aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate or DETA-NONOate #ab144627 from Abcam plc, Cambridge, UK) were the two NO donors utilised in this The IC50s of two NO donors (DETA-NO; 1250 110 M and sodium nitroprusside (SNP; 950 89 M) as well as the IC50 of H2O2 (120 7 M) were used to assess cytoprotective capacity and its underlying mechanism. Total ROS (as a collective marker of hydrogen peroxide, superoxide radical, hydroxyl radical, and other ROS) was assessed using DCFH-DA, and significant ROS was deciphered using a specialised probe DHE. The data demonstrated that signalling processes mediated primarily by and/or NO are responsible for CeO2 NPs at 100 g/mL ameliorating toxicity. The fact that NP exposure had no effect on mitochondrial membrane potential (MMP) and that CeO2 NPs-mediated recovery of MMP loss caused by exogenous NO donors and H2O2 suggested that NP-mediated generation was extra-mitochondrial. The mechanism behind the NP-induced gain in GSH and persistent cytoplasmic ROS is partially explained by data on activated glutathione reductase (GR) and unchanged glutathione peroxidase (GPx) activity. Instead of being inhibited by CeO2 NP administration, cells may develop the ability to tolerate exogenously generated toxicity due to increased antioxidant capacity due to non-cytotoxic ROS and/or NO generation.

Author(s) Details:

Mohd Javed Akhtar,
King Abdullah Institute for Nanotechnology, King Saud University, Riyadh-11451, Saudi Arabia.

Maqusood Ahamed,
King Abdullah Institute for Nanotechnology, King Saud University, Riyadh-11451, Saudi Arabia.

Please see the link here: https://stm.bookpi.org/RTCAMS-V7/article/view/6101

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