scholarly journals Cell type-specific differences in redox regulation and proliferation after low UVA doses

2018 ◽  
Author(s):  
Sylwia Ciesielska ◽  
Patryk Bil ◽  
Karolina Gajda ◽  
Aleksandra Poterala-Hejmo ◽  
Dorota Hudy ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Redox Regulation ◽  
Cellular Proliferation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cell Type ◽  
Redox Systems ◽  
Human Colon Cancer ◽  
Cellular Redox ◽  
Hct116 Cells

AbstractUltraviolet A (UVA) radiation is harmful for living organisms but in low doses may stimulate cell proliferation. Our aim was to examine the relationships between exposure to different low UVA doses, cellular proliferation, and changes in cellular reactive oxygen species levels. In human colon cancer (HCT116) and melanoma (Me45) cells exposed to UVA doses comparable to environmental, the highest doses (30-50 kJ/m2) reduced clonogenic potential but some lower doses (1 and 10 kJ/m2) induced proliferation. This effect was cell type and dose specific. In both cell lines the levels of reactive oxygen species and nitric oxide fluctuated with dynamics which were influenced differently by UVA; in Me45 cells decreased proliferation accompanied the changes in the dynamics of H2O2 while in HCT116 cells those of superoxide. Genes coding for proteins engaged in redox systems were expressed differently in each cell line; transcripts for thioredoxin, peroxiredoxin and glutathione peroxidase showed higher expression in HCT116 cells whereas those for glutathione transferases and copper chaperone were more abundant in Me45 cells. We conclude that these two cell types utilize different pathways for regulating their redox status. Many mechanisms engaged in maintaining cellular redox balance have been described. Here we show that the different cellular responses to a stimulus such as a specific dose of UVA may be consequences of the use of different redox control pathways. Assays of superoxide and hydrogen peroxide level changes after exposure to UVA may clarify mechanisms of cellular redox regulation and help in understanding responses to stressing factors.

Mitochondria-Targeted Ratiometric Fluorescent Imaging of Cysteine

The Analyst ◽  
2021 ◽  
Author(s):  
Ya-Nan Wei ◽  
Bo Lin ◽  
Yang Shu ◽  
Jian-Hua Wang
Keyword(s):  
Reactive Oxygen Species ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Fluorescent Imaging ◽  
Oxygen Species ◽  
Cellular Redox ◽  
Critical Part ◽  
Physiological Processes

As an indispensable biothiol, cysteine (Cys) plays a critical part in cellular redox homeostasis, pathological and physiological processes. One of the main sources of reactive oxygen species (ROS) in human...

scholarly journals Redox-regulation of Erk1/2-directed phosphatase by reactive oxygen species: Role in signaling TPA-induced growth arrest in ML-1 cells

2008 ◽  
Vol 216 (1) ◽  
pp. 276-285 ◽  
Author(s):  
Kassim Traore ◽  
Rajni Sharma ◽  
Rajesh K. Thimmulappa ◽  
Walter H. Watson ◽  
Shyam Biswal ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Redox Regulation ◽  
Growth Arrest ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Induction of p21 Mediated by Reactive Oxygen Species Formed during the Metabolism of Aziridinylbenzoquinones by HCT116 Cells

1996 ◽  
Vol 271 (50) ◽  
pp. 31915-31921 ◽  
Author(s):  
Xiaobo Qiu ◽  
Henry Jay Forman ◽  
Axel H. Schönthal ◽  
Enrique Cadenas
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Hct116 Cells

scholarly journals Reactive oxygen species oxidize STING and suppress interferon production

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Lili Tao ◽  
Andrew Lemoff ◽  
Guoxun Wang ◽  
Christina Zarek ◽  
Alexandria Lowe ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Redox Regulation ◽  
Reactive Oxygen ◽  
Interferon Response ◽  
Cellular Respiration ◽  
Type I ◽  
Oxygen Species ◽  
Interferon Production ◽  
Dna Sensing ◽  
Cytoplasmic Dna

Reactive oxygen species (ROS) are by-products of cellular respiration that can promote oxidative stress and damage cellular proteins and lipids. One canonical role of ROS is to defend the cell against invading bacterial and viral pathogens. Curiously, some viruses, including herpesviruses, thrive despite the induction of ROS, suggesting that ROS are beneficial for the virus. However, the underlying mechanisms remain unclear. Here, we found that ROS impaired interferon response during murine herpesvirus infection and that the inhibition occurred downstream of cytoplasmic DNA sensing. We further demonstrated that ROS suppressed the type I interferon response by oxidizing Cysteine 147 on murine stimulator of interferon genes (STING), an ER-associated protein that mediates interferon response after cytoplasmic DNA sensing. This inhibited STING polymerization and activation of downstream signaling events. These data indicate that redox regulation of Cysteine 147 of mouse STING, which is equivalent to Cysteine 148 of human STING, controls interferon production. Together, our findings reveal that ROS orchestrates anti-viral immune responses, which can be exploited by viruses to evade cellular defenses.

scholarly journals Redox Regulation and Oxidative Stress: The Particular Case of the Stallion Spermatozoa

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 567 ◽  
Author(s):  
Fernando J. Peña ◽  
Cristian O’Flaherty ◽  
José M. Ortiz Rodríguez ◽  
Francisco E. Martín Cano ◽  
Gemma L. Gaitskell-Phillips ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Redox Regulation ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Mitochondrial Activity ◽  
Oxygen Species ◽  
Redox Biology ◽  
Major Interest ◽  
And Oxidative Stress

Redox regulation and oxidative stress have become areas of major interest in spermatology. Alteration of redox homeostasis is recognized as a significant cause of male factor infertility and is behind the damage that spermatozoa experience after freezing and thawing or conservation in a liquid state. While for a long time, oxidative stress was just considered an overproduction of reactive oxygen species, nowadays it is considered as a consequence of redox deregulation. Many essential aspects of spermatozoa functionality are redox regulated, with reversible oxidation of thiols in cysteine residues of key proteins acting as an “on–off” switch controlling sperm function. However, if deregulation occurs, these residues may experience irreversible oxidation and oxidative stress, leading to malfunction and ultimately death of the spermatozoa. Stallion spermatozoa are “professional producers” of reactive oxygen species due to their intense mitochondrial activity, and thus sophisticated systems to control redox homeostasis are also characteristic of the spermatozoa in the horse. As a result, and combined with the fact that embryos can easily be collected in this species, horses are a good model for the study of redox biology in the spermatozoa and its impact on the embryo.

scholarly journals Reactive oxygen species and redox regulation in mesophyll and bundle sheath cells of C4 plants

2018 ◽  
Vol 69 (14) ◽  
pp. 3321-3331 ◽  
Author(s):  
Ismail Turkan ◽  
Baris Uzilday ◽  
Karl-Josef Dietz ◽  
Andrea Bräutigam ◽  
Rengin Ozgur
Keyword(s):  
Reactive Oxygen Species ◽  
Redox Regulation ◽  
Reactive Oxygen ◽  
Bundle Sheath ◽  
C4 Plants ◽  
Oxygen Species ◽  
Bundle Sheath Cells ◽  
Sheath Cells

scholarly journals 3-Bromopyruvate potentiates TRAIL-induced apoptosis in human colon cancer cells through a reactive oxygen species- and caspase-dependent mitochondrial pathway

2019 ◽  
Vol 97 (12) ◽  
pp. 1176-1184 ◽  
Author(s):  
Hassan Abbaszadeh ◽  
Armita Valizadeh ◽  
Masoud Mahdavinia ◽  
Ali Teimoori ◽  
Mohammad Hassan Pipelzadeh ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Human Colon ◽  
Inhibitory Effect ◽  
Oxygen Species ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Normal Cells

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a promising anticancer cytokine with minimal toxicity towards normal cells. Nevertheless, most primary cancers are often intrinsically TRAIL-resistant or can acquire resistance after TRAIL therapy. This study aimed to investigate the inhibitory effect of co-treatment of 3-bromopyruvate (3-BP) as a potent anticancer agent with TRAIL on colon cancer cells (HT-29). The results of present study indicated that combined treatment with 3-BP and TRAIL inhibited the proliferation of HT-29 cells to a greater extent (88.4%) compared with 3-BP (54%) or TRAIL (11%) treatment alone. In contrast, the combination of 3-BP and TRAIL had no significant inhibitory effect on the proliferation of normal cells (HEK-293) (8.4%). At a cellular mechanistic level, the present study showed that 3-BP sensitized human colon cancer cells to TRAIL-induced apoptosis via reactive oxygen species generation, upregulation of Bax, downregulation of Bcl-2 and survivin, release of cytochrome c into the cytosol, and activation of caspase-3. In normal cells, 3-BP, TRAIL, or combination of both had no significant effect on the reactive oxygen species levels, release of cytochrome c, and caspase-3 activity. Therefore, the combination of 3-BP and TRAIL can be a promising therapeutic strategy for treatment of colon cancer.

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