scholarly journals Hydrophilic Tetraphenylethene-Based Tetracationic Cyclophanes: NADPH Recognition and Cell Imaging With Fluorescent Switch

2021 ◽  
Vol 9 ◽  
Author(s):  
Dan Wu ◽  
Zhankui Zhang ◽  
Xinyang Yu ◽  
Bing Bai ◽  
Shaolong Qi

A hydrophilic TPE-based tetracationic cyclophane TPE-cyc was synthesized, which could capture intracellular Nicotinamide adenine dinucleotide phosphate and fuel the antioxidative ability of tumor cells to detoxify reactive oxygen species (ROS). Meanwhile, upon the reduction by cellular GSH, TPE-cyc could light up tumor cells, acting as a GSH-responsive fluorescent switch to image cells with high resolution.

2015 ◽  
Vol 35 (5) ◽  
pp. 1857-1867 ◽  
Author(s):  
Weishen Chen ◽  
Ziqing Li ◽  
Ying Guo ◽  
Yuhuan Zhou ◽  
Ziji Zhang ◽  
...  

Background/Aims: Prosthesis loosening is closely associated with chronic inflammatory cytokine secretion by macrophages, which are activated by wear particles or inflammatory stimulants such as lipopolysaccharide (LPS). Reactive oxygen species (ROS) are critical regulators of inflammation, but their enzymatic sources in response to wear particles and their effects on peri-implant LPS-tolerance remain unclear. Methods: Three ROS-related enzymes—nicotinamide adenine dinucleotide phosphate oxidase (NOX)-1 and -2 and catalase—were investigated in interface membrane tissues and in titanium (Ti) particle-stimulated macrophages in vitro. The generation of ROS and downstream inflammatory effects were measured with or without pre-incubation with apocynin, an NOX inhibitor. Results: Pre-exposure to Ti particles attenuated NF-κB activation in LPS-stimulated macrophages, indicating that wear particles suppress immune response, which may lead to chronic inflammation. NOX-1 and -2 were highly expressed in aseptically loosened interface membranes and in macrophages stimulated with Ti particles; the particles induced a moderate amount of ROS generation, NF-κB activation, and TNF-a secretion in macrophages, and these effects were suppressed by apocynin. Conclusion: Wear particles induce ROS generation through the NOX signaling pathway, resulting in persistent inflammation and delayed loosening. Thus, the suppression of NOX activity may be a useful strategy for preventing prosthesis loosening.


Endocrinology ◽  
2013 ◽  
Vol 154 (3) ◽  
pp. 1361-1372 ◽  
Author(s):  
Maria C. S. Santos ◽  
Ruy A. N. Louzada ◽  
Elaine C. L. Souza ◽  
Rodrigo S. Fortunato ◽  
Andressa L. Vasconcelos ◽  
...  

Abstract Diabetes mellitus (DM) disrupts the pituitary-thyroid axis and leads to a higher prevalence of thyroid disease. However, the role of reactive oxygen species in DM thyroid disease pathogenesis is unknown. Dual oxidases (DUOX) is responsible for H2O2 production, which is a cosubstrate for thyroperoxidase, but the accumulation of H2O2 also causes cellular deleterious effects. Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) is another member of the nicotinamide adenine dinucleotide phosphate oxidase family expressed in the thyroid. Therefore, we aimed to evaluate the thyroid DUOX activity and expression in DM rats in addition to NOX4 expression. In the thyroids of the DM rats, we found increased H2O2 generation due to higher DUOX protein content and DUOX1, DUOX2, and NOX4 mRNA expressions. In rat thyroid PCCL3 cells, both TSH and insulin decreased DUOX activity and DUOX1 mRNA levels, an effect partially reversed by protein kinase A inhibition. Most antioxidant enzymes remained unchanged or decreased in the thyroid of DM rats, whereas only glutathione peroxidase 3 was increased. DUOX1 and NOX4 expression and H2O2 production were significantly higher in cells cultivated with high glucose, which was reversed by protein kinase C inhibition. We conclude that thyroid reactive oxygen species is elevated in experimental rat DM, which is a consequence of low-serum TSH and insulin but is also related to hyperglycemia per se.


Blood ◽  
2015 ◽  
Vol 125 (2) ◽  
pp. 336-345 ◽  
Author(s):  
Zachary J. Reitman ◽  
Sergey A. Sinenko ◽  
Eric P. Spana ◽  
Hai Yan

Key Points Homologs to cancer-derived IDH1 and IDH2 mutants produce D-2HG and drive expansion of Drosophila blood cells. In flies, mutant Idh interacts with genes that regulate reduced nicotinamide adenine dinucleotide phosphate, reactive oxygen species, and apoptosis.


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