scholarly journals Microvesicle Formation Induced by Oxidative Stress in Human Erythrocytes

2020 ◽  
Author(s):  
Julia Sudnitsyna ◽  
Elisaveta Skverchinskaya ◽  
Irina Dobrylko ◽  
Elena R. Nikitina ◽  
Stepan Gambaryan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Cell Types ◽  
Band 3 ◽  
Cell Deformability ◽  
Physiological Conditions ◽  
Oxidant Concentration ◽  
Tert Butyl Hydroperoxide ◽  
Different Cell Types ◽  
And Oxidative Stress

Extracellular vesicles (EVs) released by different cell types play significant role in many physiological and pathophysiological processes. In physiological conditions red blood cells (RBCs) derived EVs compose 4 - 8% of all circulating EVs, and oxidative stress (OS) as a consequence of different pathophysiological conditions significantly increases the amount of circulated RBC-derived EVs, however the mechanisms of EV formation are not fully defined yet. To analyze OS-induced EV formation and RBCs transformations we used flow cytometry to evaluate cell esterase activity, caspase-3 activity, and band 3 clustering. Band 3 clustering was additionally analyzed by confocal microscopy. Two original laser diffraction-based approaches were used for analysis of cell deformability and band 3 activity. Hemoglobin species were characterized spectrophotometrically. We showed that cell viability in tert-butyl hydroperoxide-induced OS directly correlated with oxidant concentration to cell count ratio, RBCs-derived EVs contained hemoglobin oxidized to hemichrome (HbChr). OS induced caspase-3 activation and band 3 clustering in cells and EVs. Importantly, we showed that OS-induced EV formation is independent from calcium. Presented data indicated that during OS RBCs eliminate HbChr by vesiculation, in order to sacrifice the cell itself thereby prolonging lifespan and delaying the untimely clearance of in all other respects healthy RBCs.

scholarly journals Microvesicle Formation Induced by Oxidative Stress in Human Erythrocytes

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 929 ◽  
Author(s):  
Julia Sudnitsyna ◽  
Elisaveta Skverchinskaya ◽  
Irina Dobrylko ◽  
Elena Nikitina ◽  
Stepan Gambaryan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Cell Types ◽  
Band 3 ◽  
Cell Deformability ◽  
Physiological Conditions ◽  
Oxidant Concentration ◽  
Tert Butyl Hydroperoxide ◽  
Different Cell Types ◽  
And Oxidative Stress

Extracellular vesicles (EVs) released by different cell types play an important role in many physiological and pathophysiological processes. In physiological conditions, red blood cell (RBC)-derived EVs compose 4–8% of all circulating EVs, and oxidative stress (OS) as a consequence of different pathophysiological conditions significantly increases the amount of circulated RBC-derived EVs. However, the mechanisms of EV formation are not yet fully defined. To analyze OS-induced EV formation and RBC transformations, we used flow cytometry to evaluate cell esterase activity, caspase-3 activity, and band 3 clustering. Band 3 clustering was additionally analyzed by confocal microscopy. Two original laser diffraction-based approaches were used for the analysis of cell deformability and band 3 activity. Hemoglobin species were characterized spectrophotometrically. We showed that cell viability in tert-Butyl hydroperoxide-induced OS directly correlated with oxidant concentration to cell count ratio, and that RBC-derived EVs contained hemoglobin oxidized to hemichrome (HbChr). OS induced caspase-3 activation and band 3 clustering in cells and EVs. Importantly, we showed that OS-induced EV formation is independent of calcium. The presented data indicated that during OS, RBCs eliminated HbChr by vesiculation in order to sacrifice the cell itself, thereby prolonging lifespan and delaying the untimely clearance of in all other respects healthy RBCs.

scholarly journals Oxidative Stress, Neuroinflammation and Mitochondria in the Pathophysiology of Amyotrophic Lateral Sclerosis

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 901 ◽  
Author(s):  
Elena Obrador ◽  
Rosario Salvador ◽  
Rafael López-Blanch ◽  
Ali Jihad-Jebbar ◽  
Soraya L. Vallés ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyotrophic Lateral Sclerosis ◽  
Cell Types ◽  
T Cell Subsets ◽  
Cellular Interactions ◽  
Underlying Mechanisms ◽  
Different Cell Types ◽  
And Oxidative Stress ◽  
Different Levels ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron (MN) disease. Its primary cause remains elusive, although a combination of different causal factors cannot be ruled out. There is no cure, and prognosis is poor. Most patients with ALS die due to disease-related complications, such as respiratory failure, within three years of diagnosis. While the underlying mechanisms are unclear, different cell types (microglia, astrocytes, macrophages and T cell subsets) appear to play key roles in the pathophysiology of the disease. Neuroinflammation and oxidative stress pave the way leading to neurodegeneration and MN death. ALS-associated mitochondrial dysfunction occurs at different levels, and these organelles are involved in the mechanism of MN death. Molecular and cellular interactions are presented here as a sequential cascade of events. Based on our present knowledge, the discussion leads to the idea that feasible therapeutic strategies should focus in interfering with the pathophysiology of the disease at different steps.

Caspase-3-mediated cleavage of PHF-1 tau during apoptosis irrespective of excitotoxicity and oxidative stress: an implication to Alzheimer's disease

2005 ◽  
Vol 18 (3) ◽  
pp. 450-458 ◽  
Author(s):  
Hyo Jung Kang ◽  
Won Joo Yoon ◽  
Gyeong Joon Moon ◽  
Doo Yeon Kim ◽  
Seonghyang Sohn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caspase 3 ◽  
And Oxidative Stress

tert-Butyl hydroperoxide-induced differing plasma membrane and oxidative stress processes in yeast strains BY4741 anderg5Δ

2014 ◽  
Vol 54 (S1) ◽  
pp. S50-S62 ◽  
Author(s):  
Zoltán Gazdag ◽  
Gábor Máté ◽  
Milan Čertik ◽  
Katalin Türmer ◽  
Eszter Virág ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Membrane ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Yeast Strains ◽  
Tert Butyl Hydroperoxide ◽  
And Oxidative Stress

scholarly journals Age-associated telomere attrition of lymphocytes in vivo is co-ordinated with changes in telomerase activity, composition of lymphocyte subsets and health conditions

2014 ◽  
Vol 128 (6) ◽  
pp. 367-377 ◽  
Author(s):  
Yun Lin ◽  
Amanda Damjanovic ◽  
E. Jeffrey Metter ◽  
Huy Nguyen ◽  
Thai Truong ◽  
...  
Keyword(s):  
Lymphocyte Subsets ◽  
Length Change ◽  
Cell Types ◽  
Telomerase Activity ◽  
Health Conditions ◽  
Telomere Attrition ◽  
Physiological Conditions ◽  
Cell Percentage ◽  
Different Cell Types

The present longitudinal study reveals that the telomere length change with age in vivo differs among individuals and in different cell types and is influenced by telomerase activity, naïve T-cell percentage and changes in physiological conditions such as glucose and interleukin-6 levels.

scholarly journals MiR-122 Participates in Oxidative Stress and Apoptosis in STZ-Induced Pancreatic β Cells by Regulating PI3K/AKT Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jing Wang ◽  
Zhichun Dong ◽  
Liyin Lou ◽  
Lijuan Yang ◽  
Jingying Qiu
Keyword(s):  
Oxidative Stress ◽  
Insulin Secretion ◽  
Caspase 3 ◽  
Cell Damage ◽  
Caspase 9 ◽  
Intracellular Ros ◽  
Reverse Transcription Quantitative Pcr ◽  
Apoptosis Detection ◽  
Dichlorofluorescein Diacetate ◽  
And Oxidative Stress

At present, there are few reports concerning the relationship between miR-122 and diabetes. In addition, the effect of miR-122 on streptozotocin- (STZ-) induced oxidative damage in INS-1 cells remains unclear. The present study aimed to investigate the role and modulatory mechanisms involving miR-122 in diabetes. STZ was used to induce INS-1 cell damage. Reverse transcription-quantitative PCR was used to investigate the expression of miR-122. A TUNEL cell apoptosis detection kit was used to detect apoptosis. Intracellular ROS levels were determined using dichlorofluorescein-diacetate. The activities of insulin secretion, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-px) were measured using ELISA kits. Western blotting was used to measure the expression levels of Bax, Bcl-2, PI3K, p-PI3K, caspase-3 and caspase-9, cleaved-caspase-3 and cleaved-caspase-9, AKT, and p-AKT. Then, LY294002 (LY, PI3K inhibitor) was used to treat INS-1 cells, and oxidative stress and apoptosis were measured. The results showed that STZ-induced inhibitory effects on insulin secretion were mitigated by miR-122 inhibitor, and the activities of SOD, CAT, and GSH-px were also increased. Furthermore, miR-122 inhibitor inhibited apoptosis and oxidative stress in STZ-induced INS-1 cells. Finally, the addition of LY increased insulin levels; reduced the activities of SOD, CAT, and GSH-px; and promoted apoptosis in STZ-induced INS-1 cells. In conclusion, interference with miR-122 can inhibit oxidative stress and apoptosis in STZ-induced INS-1 cells, involving a mechanism of action related to the PI3K/AKT pathway.

Evaluation of Oxidative Stress Biomarkers in Brain Metastatic and Non-Metastatic Lung Cancer Patients with Different Cell Types

2021 ◽  
Vol 21 ◽  
Author(s):  
Emre Bilgin ◽  
Gülüzar Atli ◽  
Berna Bozkurt Duman ◽  
Ali I. Okten
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cancer Patients ◽  
Antioxidant System ◽  
Cell Types ◽  
Oxidative Stress Biomarkers ◽  
Lung Cancer Patients ◽  
Stress Biomarkers ◽  
Metastatic Lung ◽  
Different Cell Types

Background : Oxidative stress lead to an imbalanced prooxidant/antioxidant status can be a critical factor affecting the lung cancer etiopathology. The antioxidant system provides primary protection under oxidative stress. Objective: The purpose of the study was to investigate the serum antioxidant system status in brain metastatic and non-metastatic lung cancer patients with different cell types. Methods: In this prospective study, 33 patients with lung cancer metastasis (metastatic patient group), 36 lung cancer patients (non-metastatic patient group) and 25 healthy control groups were included. Enzymatic (superoxide dismutase, SOD; glutathione peroxidase, GPX; and glutathione reductase, GR) and non-enzymatic (glutathione, GSH) antioxidant system biomarkers with thiobarbituric acid reactive substances (TBARS) levels were studied in the serum samples of the control and patient groups. The oxidative stress biomarkers were measured spectrophotometrically. Results: SOD activity increased though TBARS levels and GR activity decreased in both patient groups compared to the control. GPX activity increased only in the non-metastatic group. Antioxidant biomarkers varied between small cell and non-small cell group patients. GR activity and GSH levels were significantly higher in the non-metastatic group compared to the metastatic group. There were also found correlations between antioxidant parameters in the non-metastatic group. Conclusions: It was emphasized the imbalanced antioxidant system in the duration of the disease related to not only cell type and also the metastatic structure. This is the preliminary study exhibiting the contribution of antioxidant imbalance in different subtypes with varied prognosis and behavior of lung cancer in the presence of brain metastasis. Therefore, oxidative stress biomarkers can serve as a useful tool to get information about the progression of lung cancer. Thus it may provide fundamental data for further cancer researches when considering the diagnosis of the disease.

Little change in markers of protein breakdown and oxidative stress in humans in immobilization-induced skeletal muscle atrophy

2010 ◽  
Vol 35 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Elisa I. Glover ◽  
Nobuo Yasuda ◽  
Mark A. Tarnopolsky ◽  
Arkan Abadi ◽  
Stuart M. Phillips
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Oxidative Modification ◽  
Skeletal Muscle Atrophy ◽  
Protein Carbonyls ◽  
Disuse Atrophy ◽  
Protein Breakdown ◽  
Protein Conjugates ◽  
Protein Ubiquitination ◽  
And Oxidative Stress

A number of studies in rodents suggest that disuse atrophy results from a large increase in proteolysis affected by, or accompanying, increased oxidative stress. Little information is available, however, about the effects of immobilization on markers of muscle protein breakdown and oxidative stress in humans. Therefore, the purpose of this investigation was to measure markers of breakdown or oxidative stress in subjects who underwent 14 days of knee-brace-mediated immobilization. Vastus lateralis samples taken from 21 young subjects before, and 2 days and 14 days after, single leg immobilization were measured for ubiquitin-protein conjugates, caspase 3/7 activity, the 14-kDa caspase-3 cleaved actin fragment, 4-hydroxy-2-nonenal (4-HNE) adducts, and protein carbonyls. Quadriceps cross-sectional area decreased by 5.7% ± 1.1% (p < 0.0001) following immobilization. Ubiquitin-protein conjugates were elevated at 2 days of immobilization (12%, p < 0.05) but were not different from baseline at 14 days. Levels of the 14-kDa actin fragment and caspase 3/7 activity did not change over the immobilization period. The oxidative stress markers, 4-HNE adducts and protein carbonyls, did not change at any time point. These static measures of breakdown and oxidative modification suggest that a small increase in protein ubiquitination occurs early (2 days), but elevations in ubiquitinated or oxidatively modified proteins are not sustained during the later phase (14 days) of uncomplicated disuse atrophy in humans, suggesting that these pathways are not playing a major role in simple disuse-induced atrophic loss of protein mass.

scholarly journals Influence of supplemented coated-cysteamine on morphology, apoptosis and oxidative stress status of gastrointestinal tract

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Hongnan Liu ◽  
Miaomiao Bai ◽  
Bie Tan ◽  
Kang Xu ◽  
Rong Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Control Diet ◽  
Control Group ◽  
Lesion Score ◽  
Positive Effects ◽  
Oxidative Stress Status ◽  
Mucosal Morphology ◽  
The Stability ◽  
And Oxidative Stress

Abstract Background Cysteamine was coated to cover its odor and maintain the stability. However, coated cysteamine (CC) has not been clearly evaluated for its effects on the gastrointestinal mucosa status. We hypothesize that the appropriate CC supplementation in diet impacts the stomach and intestinal mucosa variously through regulating the morphology, apoptosis, and oxidative stress status in model of pigs. Results The results showed that villus height increased (P < 0.05), and crypt depth decreased (P < 0.05) in the ileum when pigs were fed the diet with low cysteamine (LCS) compared with the control diet. The ileal lesion score in the LCS group was significantly (P < 0.01) lower than that in the control group, while the gastric lesion score in the CC group was significantly (P < 0.01) higher compared with that of the control group. It also showed that the activities of total superoxide dismutase (T-SOD) and diamine oxidase (DAO) were upregulated (P < 0.05) in the LCS group. In addition, Bax and caspase 3 immunore-activity increased (P < 0.01), and Bcl-2 immunoreactivity decreased (P < 0.01) in the gastric mucosa of pigs fed the diet with high cysteamine (HCS). The Bax and caspase 3 immunoreactivity decreased (P < 0.01), and Bcl-2 immunoreactivity increased (P < 0.01) in ileum mucosa of pigs fed the HCS diet. Conclusions Although moderate dietary coated cysteamine showed positive effects on GI mucosal morphology, apoptosis, and oxidative stress status, the excess coated cysteamine may cause apoptosis leading to GI damage in pigs.

scholarly journals How the Pathological Microenvironment Affects the Behavior of Mesenchymal Stem Cells in the Idiopathic Pulmonary Fibrosis

2020 ◽  
Vol 21 (21) ◽  
pp. 8140
Author(s):  
Martina Bonifazi ◽  
Mariangela Di Vincenzo ◽  
Miriam Caffarini ◽  
Federico Mei ◽  
Michele Salati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Chronic Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Cell Types ◽  
And Control ◽  
And Oxidative Stress

Idiopathic pulmonary fibrosis (IPF) is a chronic disease characterized by fibroblasts activation, ECM accumulation, and diffused alveolar inflammation. The role of inflammation in IPF is still controversial and its involvement may follow nontraditional mechanisms. It is seen that a pathological microenvironment may affect cells, in particular mesenchymal stem cells (MSCs) that may be able to sustain the inflamed microenvironment and influence the surrounding cells. Here MSCs have been isolated from fibrotic (IPF-MSCs) and control (C-MSCs) lung tissue; first cells were characterized and compared by the expression of molecules related to ECM, inflammation, and other interdependent pathways such as hypoxia and oxidative stress. Subsequently, MSCs were co-cultured between them and with NHLF to test the effects of the cellular crosstalk. Results showed that pathological microenvironment modified the features of MSCs: IPF-MSCs, compared to C-MSCs, express higher level of molecules related to ECM, inflammation, oxidative stress, and hypoxia; notably, when co-cultured with C-MSCs and NHLF, IPF-MSCs are able to induce a pathological phenotype on the surrounding cell types. In conclusion, in IPF the pathological microenvironment affects MSCs that in turn can modulate the behavior of other cell types favoring the progression of IPF.

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