scholarly journals Intracellular Oxidative Stress Levels are Significantly Associated with the Green Autofluorescence Intensity of Buthionine Sulfoximine-Treated B16-F10 Cells

2021 ◽  
Author(s):  
Wanzhi Tang ◽  
Weihai Ying
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Buthionine Sulfoximine ◽  
The Body ◽  
Skin Cells ◽  
Non Invasive ◽  
Skin Cell ◽  
Intracellular Ros ◽  
Intracellular Oxidative Stress ◽  
Oxidative Stress Inducer

AbstractSince oxidative stress is a critical common pathological factor of numerous diseases, it is critical to find biomarkers for non-invasive evaluations of the levels of oxidative stress in the body. Our previous studies have indicated that epidermal green autofluorescence (AF) is a novel biomarker of this type: The oxidative stress inducer buthionine sulfoximine (BSO) can dose-dependently increase the epidermal green AF of mice, with BSO doses being significantly associated with the AF intensity. However, it is necessary to use skin cell cultures to investigate the mechanisms underlying the relationships between BSO and the green AF intensity. In our current study we found that BSO concentration-dependently increased the green AF intensity of B16-F10 cells a skin cell line, with BSO concentrations being significantly associated with the AF intensity. BSO also concentration-dependently increased the intracellular DCF signals an index of ROS levels. The green AF intensity of the cells was also significantly associated with the intracellular ROS levels. Moreover, we found that the green AF intensity was significantly associated with the cell death induced by BSO. Collectively, our study has provided first evidence indicating that the green AF intensity of skin cells is significantly associated with both intracellular ROS levels and cell death of the skin cells exposed to oxidative stress, which has indicated that green AF is a novel biomarker for both oxidative stress and cell death.

scholarly journals Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

2020 ◽  
Vol 21 (7) ◽  
pp. 2501 ◽  
Author(s):  
Thomas Nury ◽  
Gérard Lizard ◽  
Anne Vejux
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Cell Death ◽  
Neurodegenerative Diseases ◽  
The Body ◽  
Protein Accumulation ◽  
Common Features ◽  
Apoptosis And Inflammation ◽  
The Brain ◽  
And Oxidative Stress

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxicity induced during the pathology, whether at the level of mitochondria, oxidative stress or apoptosis and inflammation. The conclusions of the various studies cited are oriented towards the preventive use of oils or fatty acids. The future of these lipids that can be used in therapy/prevention will undoubtedly involve a better delivery to the body and to the brain by utilizing lipid encapsulation.

scholarly journals Keratin-Based Epidermal Green Autofluorescence is a Common Biomarker of Organ Injury

2019 ◽  
Author(s):  
Mingchao Zhang ◽  
Yujia Li ◽  
Jiucun Wang ◽  
Huiru Tang ◽  
Zhong Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Ischemic Stroke ◽  
Recovery Phase ◽  
The Body ◽  
Organ Injury ◽  
Lung Cancer Patients ◽  
Non Invasive ◽  
And Oxidative Stress ◽  
Invasive Evaluation

AbstractIt is critical to discover biomarkers for non-invasive evaluation of the levels of inflammation and oxidative stress in human body - two key pathological factors in numerous diseases. Our study has indicated keratin 1-based epidermal autofluorescence (AF) as a biomarker of this type: Inducers of both inflammation and oxidative stress dose-dependently increased epidermal green AF with polyhedral structure in mice, with the AF intensity being highly associated with the dosages of the inducers. Lung cancer also induced increased epidermal green AF of mice, which was mediated by inflammation. Significant and asymmetrical increases in green AF intensity with polyhedral structure were found in the Dorsal Index Fingers’ skin of acute ischemic stroke (AIS) patients. While the AF intensity of the subjects with high risk for developing AIS, ischemic stroke patients in recovery phase and lung cancer patients was significantly higher than that of healthy controls, both AF intensity and AF asymmetry of these four groups were markedly lower than those of the AIS patients, which have shown promise for AIS diagnosis. Several lines of evidence have indicated K1 as an origin of the AF, e.g., K1 siRNA administration attenuated the oxidative stress-induced AF increase of mice. Collectively, our study has indicated K1-based epidermal AF as a biomarker for non-invasive evaluation of the levels of inflammation and oxidative stress in the body. These findings have established a basis for novel keratin’s AF-based biomedical imaging technology for non-invasive, efficient and economic diagnosis and screening of such inflammation- and oxidative stress-associated diseases as AIS.

scholarly journals Oxidative stress induces EGFR inhibition-related skin cell death

2021 ◽  
Author(s):  
Midori Morita ◽  
Mahiro Iizuka-Ohashi ◽  
Motoki Watanabe ◽  
Takumi Narita ◽  
Chikage Kato ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Egfr Inhibition ◽  
Skin Cell

scholarly journals Internalization of Titanium Dioxide Nanoparticles Is Cytotoxic for H9c2 Rat Cardiomyoblasts

Molecules ◽  
2018 ◽  
Vol 23 (8) ◽  
pp. 1955 ◽  
Author(s):  
Elizabeth Huerta-García ◽  
Iván Zepeda-Quiroz ◽  
Helen Sánchez-Barrera ◽  
Zaira Colín-Val ◽  
Ernesto Alfaro-Moreno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Death ◽  
Titanium Dioxide ◽  
Titanium Dioxide Nanoparticles ◽  
Membrane Integrity ◽  
The Body ◽  
Potential Health ◽  
Tio2 Nps

Titanium dioxide nanoparticles (TiO2 NPs) are widely used in industry and daily life. TiO2 NPs can penetrate into the body, translocate from the lungs into the circulation and come into contact with cardiac cells. In this work, we evaluated the toxicity of TiO2 NPs on H9c2 rat cardiomyoblasts. Internalization of TiO2 NPs and their effect on cell proliferation, viability, oxidative stress and cell death were assessed, as well as cell cycle alterations. Cellular uptake of TiO2 NPs reduced metabolic activity and cell proliferation and increased oxidative stress by 19-fold measured as H2DCFDA oxidation. TiO2 NPs disrupted the plasmatic membrane integrity and decreased the mitochondrial membrane potential. These cytotoxic effects were related with changes in the distribution of cell cycle phases resulting in necrotic death and autophagy. These findings suggest that TiO2 NPs exposure represents a potential health risk, particularly in the development of cardiovascular diseases via oxidative stress and cell death.

scholarly journals PTH Protects Osteocytes From Oxidative Stress and Cellular Senescence

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A239-A239
Author(s):  
Yuhei Uda ◽  
Roberto Santos ◽  
Alejandro Kochen ◽  
Carly Newell ◽  
Tim Y Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Cellular Senescence ◽  
Intracellular Ros ◽  
Antioxidant Function ◽  
Skeletal Homeostasis ◽  
In Cells

Abstract Age-induced osteoporosis is characterized by a progressive decline in bone formation and increase in bone resorption with uncoupled activities of osteoblasts and osteoclasts. Parathyroid hormone (PTH) is used in the clinic to treat osteoporosis due to its anabolic actions on bone via binding to the PTH receptor (PPR). The receptor is highly expressed in cells of the osteoblastic lineage, including osteocytes. Osteocytes are the most abundant cells in bone and serve as a key regulator of bone remodeling. Despite the significant role of PPR signaling in skeletal homeostasis, its function in osteocytes during aging remains unclear. We have gathered preliminary data demonstrating that mice lacking PPR predominantly in osteocytes (Dmp1-PPRKO) have marked age-induced bone loss due to increased bone resorption and suppressed bone formation. These mice, with aging, develop characteristics of skeletal senescence: a decrease in osteoprogenitors and an increase in bone marrow adiposity and p16Ink4a/Cdkn2a expression in bone. Since senescence of cells in the bone microenvironment has been reported as a cause of age-induced bone loss, we hypothesized that PPR signaling protects osteocytes from senescence. To test this hypothesis, we generated osteocytes (Ocy454-12H), in which the PPR expression was ablated using CRISPR/Cas9 technique. Ocy454-12H-PPRKO and Ocy454-12H-PPRCtrl cells were treated with PTH followed by an exposure to hydrogen peroxide (H2O2). High levels of intracellular reactive oxygen species (ROS), including H2O2, promote protein and DNA oxidation, resulting in cell death and senescence. PTH treatment significantly suppressed the increase in H2O2-induced cell death, measured by resazurin-based assays, in PPRCtrl but not in PPRKO cells. We analyzed intracellular ROS levels using a fluorescent probe and found that PTH treatment significantly suppressed the increase in ROS upon H2O2 exposure, suggesting an antioxidant function of PTH in osteocytes. To further investigate if PTH prevents osteocytes from oxidative stress-induced senescence, we examined senescence-associated β-galactosidase (SA β-gal) activity in cells that were treated with PTH followed by an exposure to low doses of H2O2. Compared to untreated and PPRKO groups, treatment with PTH significantly decreased the number of SA β-gal positive cells, demonstrating that PPR signaling protects osteocytes, and possibly other osteoblastic cells, from H2O2-induced cellular senescence. PTH treatment reduced mRNA expression of p21/Cdkn1a. Taken together these results demonstrate that PPR signaling is important to protect osteocytes from cellular senescence.

Induction of Oxidative Stress and Glutathione Depletion by ABT-737, a Novel Small Molecule Inhibitor of Bcl-2, Contributes to Cytotoxicity in Leukemia Cells.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4336-4336
Author(s):  
Joya Chandra ◽  
Adrienne Howard ◽  
Kathleen Jensen ◽  
Ray Meyn
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Small Molecule ◽  
Buthionine Sulfoximine ◽  
Redox Status ◽  
Lymphocytic Leukemia ◽  
Glutathione Depletion ◽  
Dose Dependent Increase ◽  
Dose Dependent

Abstract The Bcl-2 family of proteins regulate the process of cell death. Bcl-2 and Bcl-xL are potent anti-apoptotic members that are overexpressed in a number of malignancies, providing a means to evade cell death, which has been described as a characteristic hallmark of cancer. Several lines of evidence suggest that Bcl-2 and Bcl-xL possess anti-oxidant properties. Overexpression of Bcl-2 is protective against menadione and hydrogen peroxide induced cell death and causes an increase in intracellular levels of glutathione (GSH), the most abundant antioxidant defense. In the present study, we utilized a novel small molecule to test effects of Bcl-2 inhibition on intracellular redox status. ABT-737 is a first generation inhibitor of Bcl-2, Bcl-xL and Bcl-w and and acts as a mimic of the BH3-only antagonists of these family members. Exposure of acute lymphocytic leukemia (ALL) cells to ABT-737 caused a dose dependent increase in intracellular levels reactive oxygen species (ROS), namely superoxide and hydrogen peroxide. This dose dependent increase in intracellular oxidants was significantly less pronounced in cells treated with the less active enantiomer of ABT-737. A greater than 50% decrease in intracellular GSH levels was seen with similar doses of ABT-737 and the combination of buthionine sulfoximine, an agent that depletes GSH levels further, with ABT-737, caused synergistic cell death. These data were verified using cells transfected with a tetracycline repressable Bcl-2 expression plasmid. Taken together, our data identifies a novel sequelae for Bcl-2 inhibition: the induction of oxidative stress. Combination therapies utilizing ABT-737 or its analogs may be devised based on the observed effects on the redox environment.

scholarly journals Hydrogen Peroxide Causes Cell Death via Increased Transcription of HOXB13 in Human Lung Epithelial A549 Cells

Toxics ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 78
Author(s):  
Naoki Endo ◽  
Takashi Toyama ◽  
Akira Naganuma ◽  
Yoshiro Saito ◽  
Gi-Wook Hwang
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Human Lung ◽  
A549 Cells ◽  
Protein Levels ◽  
Intracellular Ros ◽  
Lung Epithelial ◽  
Homeobox Protein

Although homeobox protein B13 (HOXB13) is an oncogenic transcription factor, its role in stress response has rarely been examined. We previously reported that knockdown of HOXB13 reduces the cytotoxicity caused by various oxidative stress inducers. Here, we studied the role of HOXB13 in cytotoxicity caused by hydrogen peroxide in human lung epithelial A549 cells. The knockdown of HOXB13 reduced hydrogen peroxide-induced cytotoxicity; however, this phenomenon was largely absent in the presence of antioxidants (Trolox or N-acetyl cysteine (NAC)). This suggests that HOXB13 may be involved in the cytotoxicity caused by hydrogen peroxide via the production of reactive oxygen species (ROS). Hydrogen peroxide also increased both the mRNA and protein levels of HOXB13. However, these increases were rarely observed in the presence of a transcriptional inhibitor, which suggests that hydrogen peroxide increases protein levels via increased transcription of HOXB13. Furthermore, cell death occurred in A549 cells that highly expressed HOXB13. However, this cell death was mostly inhibited by treatment with antioxidants. Taken together, our findings indicate that HOXB13 may be a novel factor involved in the induction of oxidative stress, which causes cell death via intracellular ROS production.

scholarly journals Effect of Pholiota nameko Polysaccharides Inhibiting Methylglyoxal-Induced Glycation Damage In Vitro

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1589
Author(s):  
His Lin ◽  
Ting-Yun Lin ◽  
Jer-An Lin ◽  
Kuan-Chen Cheng ◽  
Shella Permatasari Santoso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
Water Extract ◽  
Raw Material ◽  
Pholiota Nameko ◽  
Skin Cell ◽  
Intracellular Ros ◽  
Glycation End Products ◽  
Induced Changes

Advanced glycation end products (AGEs) can induce oxidative stress and inflammation. AGEs are major risk factors for the development of many aging-related diseases, such as cancer and diabetes. In this study, Pholiota nameko polysaccharides (PNPs) were prepared from water extract of P. nameko via graded alcohol precipitation (40%, 60%, and 80% v/v). We explored the in vitro antiglycation ability of the PNPs and inhibition of methylglyoxal (MG)-induced Hs68 cell damage. In a bovine serum albumin (BSA) glycation system, PNPs significantly inhibited the formation of Amadori products. Fluorescence spectrophotometry revealed that the PNPs trapped MG and reduced MG-induced changes in functional groups (carbonyl and ε-NH2) in the BSA. Pretreating Hs68 cells with PNPs enhanced the cell survival rate and protected against MG-induced cell damage. This was due to decreased intracellular ROS content. PNPs thus mitigate skin cell damage and oxidative stress resulting from glycation stress, making them a potential raw material for antiaging-related skincare products.

scholarly journals Assessment of Lemon Balm (Melissa officinalisL.) Hydrogels: Quality and Bioactivity in Skin Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Kristina Ramanauskienė ◽  
Ada Stelmakiene ◽  
Daiva Majienė
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Rosmarinic Acid ◽  
Stress Conditions ◽  
Ros Generation ◽  
Lemon Balm ◽  
Skin Cells ◽  
Biological Studies ◽  
Intracellular Ros

Theaimof the study was to design gels with lemon balm extract, assess their quality, and investigate the effect of rosmarinic acid on skin cells in normal conditions and under oxidative stress.Methods. The quantities of rosmarinic acid (RA) released from gels were evaluated by applying the HPLC technique. HaCaT cell viability was assessed by using the MTT method. ROS generation was measured using DCFH-DA dye. Theresultsshowed that the gelling material affected the release of RA content from gels. Lower and slower RA content release was determined in carbomer-based gels. After 6 hours of biopharmaceutical researchin vitro, at least 4% of RA was released from the gel. The results of the biological studies on HaCaT cells demonstrated that, in the oxidative stress conditions, RA reduced intracellular ROS amounts to 28%; 0.25–0.5 mg/mL of RA increased cell viability by 10–24% and protected cells from the damage caused by H2O2.Conclusions. According to research results, it is appropriate to use a carbomer as the main gelling material, and its concentration should not exceed 1.0%. RA, depending on the concentration, reduces the amount of intracellular ROS and enhances cell viability in human keratinocytes in oxidative stress conditions.

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