scholarly journals Cell-biological effects of zinc oxide spheres and rods from the nano- to the microscale at sub-toxic levels

Author(s):  
M. Olejnik ◽  
M. Kersting ◽  
N. Rosenkranz ◽  
K. Loza ◽  
M. Breisch ◽  
...  

AbstractZinc oxide particles were synthesized in various sizes and shapes, i.e., spheres of 40-nm, 200-nm, and 500-nm diameter and rods of 40∙100 nm2 and 100∙400 nm2 (all PVP-stabilized and well dispersed in water and cell culture medium). Crystallographically, the particles consisted of the hexagonal wurtzite phase with a primary crystallite size of 20 to 100 nm. The particles showed a slow dissolution in water and cell culture medium (both neutral; about 10% after 5 days) but dissolved within about 1 h in two different simulated lysosomal media (pH 4.5 to 4.8). Cells relevant for respiratory exposure (NR8383 rat alveolar macrophages) were exposed to these particles in vitro. Viability, apoptosis, and cell activation (generation of reactive oxygen species, ROS, release of cytokines) were investigated in an in vitro lung cell model with respect to the migration of inflammatory cells. All particle types were rapidly taken up by the cells, leading to an increased intracellular zinc ion concentration. The nanoparticles were more cytotoxic than the microparticles and comparable with dissolved zinc acetate. All particles induced cell apoptosis, unlike dissolved zinc acetate, indicating a particle-related mechanism. Microparticles induced a stronger formation of reactive oxygen species than smaller particles probably due to higher sedimentation (cell-to-particle contact) of microparticles in contrast to nanoparticles. The effect of particle types on the cytokine release was weak and mainly resulted in a decrease as shown by a protein microarray. In the particle-induced cell migration assay (PICMA), all particles had a lower effect than dissolved zinc acetate. In conclusion, the biological effects of zinc oxide particles in the sub-toxic range are caused by zinc ions after intracellular dissolution, by cell-to-particle contacts, and by the uptake of zinc oxide particles into cells.

2012 ◽  
Vol 544 ◽  
pp. 67-72 ◽  
Author(s):  
Lanqin Tang ◽  
Xuefeng Ding ◽  
Xu Zhao ◽  
Zichen Wang ◽  
Bing Zhou

2012 ◽  
Vol 1413 ◽  
Author(s):  
Zuzanna. A. Lewicka ◽  
Vicki. L. Colvin

ABSTRACTNanosized titanium dioxide (TiO2) and zinc oxide (ZnO) are widely used as inorganic sunscreen pigments. However, these metal oxide particles may also be photocatalytic and generate DNA-damaging reactive oxygen species. Therefore, we evaluated the photochemical properties of the whole sunscreen emulsions that contained nanoscale components and the inorganic particles derived from these sunscreens using several assays such as dichlorofluorescein fluorescence, the decolorization of Congo red dye and DMPO spin trap electron paramagnetic resonant spectroscopy. The results of these three tests showed that samples with ZnO nanoscale materials were more photoactive than the samples that contained TiO2 nanoparticles.


Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1968
Author(s):  
Yun-Jeong Ji ◽  
Sujin Kim ◽  
Jwa-Jin Kim ◽  
Gwi Yeong Jang ◽  
Minho Moon ◽  
...  

(1) Background: Although Platycodon grandiflorum saponins exhibit many beneficial biological effects in various diseases and conditions, how they protect nerve cells against neurodegenerative diseases and Alzheimer’s disease (AD) pathology is unknown. We investigated whether P. grandiflorum crude saponin (PGS) protects neurons from neurodegeneration caused by amyloid beta (Aβ)-induced oxidative stress. (2) Methods: Hippocampal neuron HT-22 cells were used in the in vitro experiment, and AD mice (5XFAD mice) were used as the in vivo model. Intracellular reactive oxygen species (ROS) was stained with DCF-DA and assessed using fluorescence microscopy. To elucidate the mechanism underlying neuroprotection, intracellular protein levels were assessed by western blotting. In 5XFAD mice, an animal model of AD, nerve damage recovery due to the induction of Aβ toxicity was evaluated by histological analysis. (3) Results: PGS attenuates Aβ-induced neurotoxicity by inhibiting Aβ-induced reactive oxygen species (ROS) production and apoptosis in HT-22 cells. Furthermore, PGS upregulated Nrf2-mediated antioxidant signaling and downregulated NF-κB-mediated inflammatory signaling. Additionally, PGS inhibited apoptosis by regulating the expression of apoptosis-associated proteins. In addition, PGS ameliorated Aβ-mediated pathologies, leading to AD-associated cognitive decline. (4) Conclusions: Taken together, these findings suggest that PGS inhibits Aβ accumulation in the subiculum and cerebral cortex and attenuates Aβ toxicity-induced nerve damage in vitro and in vivo. Therefore, PGS is a resource for developing AD therapeutics.


2021 ◽  
Vol 17 (12) ◽  
pp. 2420-2432
Author(s):  
Shichen Xie ◽  
Jingyao Zhu ◽  
Dicheng Yang ◽  
Yan Xu ◽  
Jun Zhu ◽  
...  

With wide application of Zinc oxide (ZnO) nanoparticles, their biological toxicity has received more and more attention in recent years. In this research, two ZnO dispersions with different particle sizes, small size Zinc oxide (S-ZnO) and big size Zinc oxide (B-ZnO), were prepared using polycarboxylic acid as dispersant. We found that the S-ZnO nanoparticles showed stronger toxicity on Human Pulmonary Alveolar Epithelial Cells (HPAEpiC) under same concentration. Only 9 ppm S-ZnO could decrease HPAEpiC viability to about 50%, which means that, a small amount of well-dispersed ZnO nanoparticles in industrial production process may cause serious damage to the human body through oral inhalation. Focusing on mechanism for cytotoxicity, ZnO nanoparticles promoted generation and accumulation of Reactive Oxygen Species (ROS) in mitochondria via inhibiting Superoxide Dismutase (SOD) enzyme activity and reducing Glutathione (GSH) content. ROS in turn opened the mitochondrial Ca2+ pathway and lowered the Mitochondrial Membrane Potentials (MMP), leading to cell death. To simulate the lung environment in vitro, mixed dipalmitoyl phosphatidylcholine (DPPC) and ZnO nanoparticles (1:1) were incubated for 72 hours and then cytotoxicity was evaluated on HPAEpiC. Results showed that the cell viability was significantly increased, which proved that the DPPC effectively inhibited the toxicity of ZnO nanoparticles.


2019 ◽  
Vol 49 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Kwang Hoon Seo ◽  
Josua Markus ◽  
Veronika Soshnikova ◽  
Keun Hyun Oh ◽  
Gokulanathan Anandapadmanaban ◽  
...  

2019 ◽  
Vol 20 (21) ◽  
pp. 5380 ◽  
Author(s):  
Brahim Arkoun ◽  
Ludovic Galas ◽  
Ludovic Dumont ◽  
Aurélie Rives ◽  
Justine Saulnier ◽  
...  

Freezing–thawing procedures and in vitro culture conditions are considered as a source of stress associated with increased reactive oxygen species (ROS) generation, leading to a damaged cell aerobic metabolism and consequently to oxidative stress. In the present study, we sought to investigate whether vitamin E (Vit E) or reduced glutathione (GSH) enhances sperm production by decreasing ROS accumulation during in vitro maturation of prepubertal mice testes. Testes of prepubertal mice were cryopreserved using a freezing medium supplemented or not supplemented with Vit E and were cultured after thawing. In presence of Rol alone in culture medium, frozen-thawed (F-T) testicular tissues exhibited a higher ROS accumulation than fresh tissue during in vitro culture. However, Vit E supplementation in freezing, thawing, and culture media significantly decreased cytoplasmic ROS accumulation in F-T testicular tissue during in vitro maturation when compared with F-T testicular tissue cultured in the presence of Rol alone, whereas GSH supplementation in culture medium significantly increased ROS accumulation associated with cytolysis and tissue disintegration. Vit E but not GSH promoted a better in vitro sperm production and was a suitable ROS scavenger and effective molecule to improve the yield of in vitro spermatogenesis from F-T prepubertal mice testes. The prevention of oxidative stress in the cytoplasmic compartment should be regarded as a potential strategy for improving testicular tissue viability and functionality during the freeze–thaw procedure and in vitro maturation.


Author(s):  
E. R. Kudoyarov ◽  
D. D. Karimov ◽  
D. O. Karimov ◽  
E. F. Repina ◽  
A. B. Bakirov ◽  
...  

Introduction. One of the stages of the pathogenesis of the toxic eff ect of carbon tetrachloride is the formation of compounds of reactive oxygen species with DNA, leading to the modifi cation of nitrogenous bases. The frequency of formation of nucleotides modifi ed by nitrogenous bases correlates with the number of single-and double-chain breaks of deoxyribonucleic acid (DNA) molecules. The initiator of the formation of active forms of oxygen and lipid peroxidation in liver cells upon receipt of carbon tetrachloride is a trichloromethyl radical formed during biotransformation by microsomal enzymes of cytochrome P450.The aim of the study was to analyze the changes in the genotoxicity of carbon tetrachloride in hepatocytes at normal and increased activity of cytochrome P450 caused by the infl uence of an inductor (sovol).Materials and methods. Evaluation of genotoxicity is performed by the method of DNA-comets aft er gavage with carbon tetrachloride culture of mouse hepatocytes МН22а in 96-well microplates without the induction of cytochrome P450 and chemical induction of cytochrome P450 by sovol. Determination of DNA content in comet tail (%), comet tail length (μm) and tail moment was performed in ImageJ 1.48. Statistical analysis of the results was performed in the program SPSS Statistics 21.Results: Experimental data on the genotoxic eff ect of carbon tetrachloride on hepatocytes of the MN–22A cell line without induction of cytochrome P450 and chemical induction of cytochrome P450 by sovol are presented. It was found that 0.5 mm solution of carbon tetrachloride in 1 hour aft er addition to the culture medium is genotoxic for hepatocytes MH–22a without the use of sovol (p<0.001). Th e lack of determined using the method of DNA-comet signs of genotoxicity of 5 mm carbon tetrachloride (p>0.05) in the culture medium, probably due to the transition of the cells into a state of parametros. Genotoxic eff ect is not detected by DNA comet aft er 3 and 24 hours of incubation of hepatocytes MN–22A with 0.5 and 5 mm solutions of carbon tetrachloride without preincubation with sovol (p>0.05), which may indicate repair of the damage. Aft er 72 hours of preliminary incubation of hepatocytes with sovol and the followin g four-hour cell priming with 2.5 mm tetrachloromethane solution, higher values of the parameters of DNA comets are observed than when seeding with tetrachloromethane without incubation with sovol (p<0.05).Conclusions: According to the results of the study 72 hours of cytochrome P450 induction by sovol increases the genotoxicity of carbon tetrachloride in vitro, compared with 24 h of inductor exposure, which may indirectly indicate a higher level of formed reactive oxygen species caused by increased activity of cytochrome P450 enzymes. 


Sign in / Sign up

Export Citation Format

Share Document