5 research outputs found
Evaluating Single-Cell DNA Damage Induced by Enhanced Radiation on a Gold Nanofilm Patch
Although
radiotherapy is a general oncology treatment and is often synergistically
applied with surgery and chemotherapy, it can cause side effects during
and after treatment. Gold nanoparticles were studied as a potential
material to enhance radiation to induce damage in cancer cells. However,
few studies have been conducted to examine the effects of gold nanofilm
on cell impairment under X-ray treatment. This paper describes a microfabrication-based
single-cell array platform to evaluate DNA damage induced by enhanced
X-ray radiation on gold nanofilm patches (GNFPs). Cancer cells were
patterned on GNFPs of different diameters and thicknesses, where each
cell was attached on one GNFP. The end-point DNA damage induced by
X-ray was examined in situ at the single-cell level using a halo assay.
The preliminary data demonstrated that the enhancement of DNA damage
was significantly related to the area and thickness of the GNFP. This
platform may be hopefully used to establish the mathematical relationships
among DNA damage, X-ray dosage, and thickness and area of the GNFP,
and further contribute to radiation dosage screening for personalized
radiotherapy
Consecutive evaluation of graphene oxide and reduced graphene oxide nanoplatelets immunotoxicity on monocytes
Nano zerovalent iron particles induce pulmonary and cardiovascular toxicity in an in vitro human co-culture model
Despite promising environmental applications for nano zerovalent iron (nZVI), concerns remain about the potential accumulation and toxic effects of nZVI particles. Here, we use an alveolar-capillary co-culture model to investigate a possible link between low-level epithelial exposure to nZVI and pulmonary and cardiovascular toxicity. While nZVI was unable to pass through the epithelial barrier into the endothelium, nZVI exposure did cause oxidative and inflammatory responses in both epithelial and endothelial cells. Therefore, toxic effects induced by nZVI are not restricted to epithelial cells but can be transferred into the endothelium. Communication between A549 and EA.hy926 cells is responsible for amplification of nZVI-induced toxic responses. Decreases in transepithelial electrical resistance and zonula occludens proteins after epithelial exposure to nZVI impaired epithelial barrier integrity. Increases in oxidized 1-antitrypsin and oxidized low-density lipoprotein in the co-culture model suggest that nZVI exposure increases the risk of chronic obstructive pulmonary disease and atherosclerosis. Therefore, inhalation of nZVI has the potential to induce cardiovascular disease through oxidative and inflammatory mediators produced from the damaged lung epithelium in chronic lung diseases