The effect of increasing temperature on Hsp60 expression, oxidative stress, antioxidants, electrolyte changes and apoptosis in broiler blood cells in-vitro

2021 ◽  
Author(s):  
W. Aengwanich* ◽  
J. Wandee
Keyword(s):  
Oxidative Stress ◽  
Blood Cells ◽  
Hsp60 Expression ◽  
Increasing Temperature

Protective effect of quercetin in gentamicin-induced oxidative stress in vitro and in vivo in blood cells. Effect on gentamicin antimicrobial activity

2016 ◽  
Vol 48 ◽  
pp. 253-264 ◽  
Author(s):  
Pamela Soledad Bustos ◽  
Romina Deza-Ponzio ◽  
Paulina Laura Páez ◽  
Ines Albesa ◽  
José Luis Cabrera ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antimicrobial Activity ◽  
Protective Effect ◽  
Blood Cells

Increased susceptibility of microcytic red blood cells to in vitro oxidative stress

2009 ◽  
Vol 55 (5) ◽  
pp. 327-331 ◽  
Author(s):  
J. L. Vives Corrons ◽  
A. Miguel-Garcia ◽  
M. A. Pujades ◽  
A. Miguel-Sosa ◽  
S. Cambiazzo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Increased Susceptibility

Oxidative Stress and Increased Destruction of Red Blood Cells Contribute to the Pathophysiology of Anemia Caused By DMT1 Deficiency

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4027-4027 ◽  
Author(s):  
Zuzana Zidova ◽  
Daniel Garcia-Santos ◽  
Katarina Kapralova ◽  
Pavla Koralkova ◽  
Renata Mojzikova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Fetal Liver ◽  
Erythroid Differentiation ◽  
Heme Oxygenase 1 ◽  
Wild Type ◽  
Divalent Metal Transporter 1 ◽  
Oxidative Defense

Abstract Inactivating mutations in divalent metal transporter 1 (DMT1) are associated with a severe defect in erythroid iron utilization and cause moderate to severe hypochromic microcytic anemia in human patients and two rodent models. We have previously shown that DMT1 deficiency impairs erythroid differentiation, induces apoptosis of erythroid precursors and causes the suppression of colony-forming capacity of erythroid progenitors. Using in vitro cultures of fetal liver cells we were able to recapitulate this in vivo defect. We confirmed abnormal pattern of erythroid differentiation and increased apoptosis (2.5-times) of DMT1-mutant erythroblasts when compared to wild-type (wt) fetal liver erythroblats. Determination of 2’,7’-Dichlorofluorescein diacetate-dependent intensity of fluorescence, which is proportional to the concentration of reactive oxygen species (ROS), revealed elevated levels of ROS in DMT1-mutant erythroblats when compared to wt erythroblast. This result suggests that oxidative stress contributes to the apoptosis in DMT1-mutant cells. We also observed that the defective erythroid differentiation of DMT1-mutant erythroblasts is marked by a blunted induction of heme oxygenase-1, an enzyme that co-regulates erythroid differentiation by controlling the heme regulatory pool in erythroid cells (Garcia-Santos et al., Blood, 2014, 123 (14): 2269-77). In further studies we focused on mature red blood cells (RBC), because it is known that nutritional iron deficiency and certain types of congenital hypochromic anemia are associated with increased levels of ROS and shortened life span of RBC that can be at least partially attributed to a programmed cell death of erythrocytes, so called eryptosis (Lang et al., Int J Biochem Cell Biol, 2012, 44 (8): 1236-43). Using labeling with carboxyfluorescein diacetate succinimidyl ester, we observed an accelerated clearance of DMT1-mutant RBC from circulating blood when compared to wild-type RBC. In vitro, DMT1-mutant RBC exposed to hyperosmotic shock or glucose depletion showed significantly increased levels of phosphatidylserine on the membrane detected by Annexin V binding. Together, these results confirmed eryptosis of DMT1-mutant RBC. As eryptosis is proposed to be triggered via activation of Ca2+ cation channels, we next measured the concentration of cytosolic Ca2+ using Fluo3/AM fluorescent dye and found significantly elevated content of intracellular Ca2+ in DMT1-mutant RBC when compared to wt RBC. In addition, DMT1-mutant RBC had higher levels of ROS than wt RBC despite significantly increased activity of anti-oxidative defense enzymes; glutathione peroxidase (1.6-times), catalase (1.9-times) and methemoglobin reductase (1.9-times). This indicates that exaggerated anti-oxidative defense in DMT1-mutant RBC is not sufficient to eliminate ROS effectively. Furthermore, DMT1-mutant RBC also showed accelerated anaerobic glycolysis as detected by increased activities of hexokinase (2.5-times), pyruvate kinase (2.4-times), glucose-phosphate isomerase (3.2-times). This result together with reduced ATP/ADP (1.6-times) ratio in DMT1-mutant RBC when compared to wt RBC suggests an increased demand for ATP in DMT1-mutant erythrocytes. In conclusion we propose that increased oxidative stress and accelerated destruction of RBC contribute to the pathophysiology of anemia caused by DMT1-deficiency. Grant support: Czech Grant Agency, grant No. P305/11/1745; Ministry of Health Czech Republic, grant No. NT13587, Education for Competitiveness Operational Program, CZ.1.07/2.3.00/20.0164, Internal Grant of Palacky University Olomouc, LF_2014_011 and in part by the Canadian Institutes of Health Research (D.G-S., P.P.). Disclosures No relevant conflicts of interest to declare.

Oxidative Stress in Red Blood Cells, Platelets and Polymorphonuclear Leukocytes from Patients with Myelodysplastic Syndrome.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2632-2632
Author(s):  
Eitan Fibach ◽  
Hussam Ghoti ◽  
Johnny Amer ◽  
Asher Winder ◽  
Eliezer Rachmilewitz
Keyword(s):  
Oxidative Stress ◽  
Myelodysplastic Syndrome ◽  
Blood Cells ◽  
Cell Damage ◽  
Iron Chelator ◽  
Oxidative Status ◽  
Iron Chelators ◽  
Ros Generation ◽  
Transfusion Requirements

Abstract Myelodysplastic syndrome (MDS) is characterized by refractory cytopenias due to ineffective hematopoiesis. Some patients with severe anemia require multiple blood transfusions and develop iron overload. Consequently, reactive oxygen species (ROS) are generated concomitant with a decrease in cellular antioxidants such as reduced gluthatione (GSH). The generated oxidative stress contributes to cell damage, apoptosis and ineffective hematopoiesis. Using flow cytometry, we measured the oxidative state of RBC, platelets and PMN in 14 low-risk MDS patients and 25 normal donors. The results indicate that the majority of the patients had higher ROS in RBC (2.79-fold) and platelets (2.91-fold) and lower GSH in their RBC (3.4-fold) and platelets (2.1-fold) than normal (p<0.005). As for PMN, there were no significant differences in ROS, although GSH was significantly (p<0.1) lower in MDS compared with normal donors. The oxidative stress in MDS cells could be ameliorated by a short in vitro treatment with the iron-chelators deferrioxamine and deferiprone, or with the anti-oxidant N-acetylcysteine. These results suggest that the decrease in transfusion requirements with increase in platelet and PMN counts in MDS patients treated with deferrioxamine may be due to indirect antioxidant effect of the iron chelator and suggest that treatment with a combination of iron-chelators and anti-oxidants might be more effective. ROS generation and GSH content in MDS blood cells ROS generation and GSH content in MDS blood cells Effect of iron chelations and an antioxidant on the oxidative status of MDS cells Effect of iron chelations and an antioxidant on the oxidative status of MDS cells

scholarly journals Protective Effect of Pitao (Pitavia punctata (R. & P.) Molina) Polyphenols against the Red Blood Cells Lipoperoxidation and the In Vitro LDL Oxidation

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ricardo I. Castro ◽  
Oscar Forero-Doria ◽  
Luis Soto-Cerda ◽  
A. Peña-Neira ◽  
Luis Guzmán
Keyword(s):  
Oxidative Stress ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Hypochlorous Acid ◽  
Low Density Lipoprotein ◽  
Membrane Integrity ◽  
Density Lipoprotein ◽  
Ldl Oxidation ◽  
Quercetin Derivatives

The oxidative stress is characterized by an imbalance between the oxidizing agents and antioxidants; meanwhile, the consumption of antioxidants has been considered as an important tool in the prevention of oxidative stress and its consequences. Pitavia punctata (R. & P.) Molina is an endemic arboreal species from the Chilean Coast Range, in which a large amount of flavonoids has been described. This work focused on characterizing and evaluating, in human erythrocytes, the antioxidant capacity and membrane protection of P. punctata extracts and the in vitro protection of the oxidation of the Low Density Lipoprotein (LDL). The phytochemical screening revealed the presence of Quercetin derivatives and flavonoids, such as (-)-Epicatechin, Kaempferol, and derivatives. The methanolic extract presented an important antioxidant activity, protecting the membrane integrity of the red blood cells against the oxidative damage caused by Hypochlorous acid and inhibiting the oxidation of the LDL lipoprotein.

Boron Compounds Counteracts Oxidative Stress Mediated Genotoxicity Induced by Fe3O4 Nanoparticles In Vitro

2016 ◽  
Vol 835 ◽  
pp. 84-90 ◽  
Author(s):  
Hasan Türkez ◽  
Erdal Sönmez ◽  
Abdulgani Tatar
Keyword(s):  
Oxidative Stress ◽  
Boric Acid ◽  
Antioxidant Capacity ◽  
Blood Cells ◽  
Defense Mechanisms ◽  
Human Lymphocytes ◽  
Protective Role ◽  
Boron Compounds

Due to rapid growing of nanotechnology, it is currently being used in many areas including biotechnology, electronics, drug delivery systems, cosmetics, material science and biosensors. Oxidative stress is considered as main cause behind the toxicity of nanoparticles (NPs). Recent reports indicate that boron is effective in protecting cells or organisms against oxidative damages by enhancing antioxidant defense mechanisms. However, protective role of boron compounds in nanotoxicity is not investigated yet. Therefore we assessed the potential protective role of boric acid (BA) and borax (BX) against the toxic responses of nano-Fe3O4 particles (IO NPs) in cultured human whole blood cells. Our results showed that IO NPs induced genotoxicity in human lymphocytes demonstrated by sister chromatid exchange (SCE) and 8-hydroxy-2′-deoxyguanosine (8-OH-dG) assays. Again, IO NPs caused decreases of total antioxidant capacity (TAC) and decreases of total oxidative stress (TOS) levels in vitro. Co-application of boric acid and borax (2.5 to 10 ppm) into the cell cultures significantly ameliorated genotoxicity and oxidative stress caused by IO NPs. In a conclusion, this study is the first report revealing that BA and BX significantly protected human blood cells from the toxicity of IO NPs, which is mediated through the generation of oxidative stress and depletion of antioxidant capacity.

scholarly journals Microfluidic Characterization of Red Blood Cells Microcirculation under Oxidative Stress

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3552
Author(s):  
Nadezhda A. Besedina ◽  
Elisaveta A. Skverchinskaya ◽  
Alexander S. Ivanov ◽  
Konstantin P. Kotlyar ◽  
Ivan A. Morozov ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Side Effects ◽  
Gas Exchange ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Microfluidic Devices ◽  
Tert Butyl Hydroperoxide ◽  
Hematological Analysis

Microcirculation is one of the basic functional processes where the main gas exchange between red blood cells (RBCs) and surrounding tissues occurs. It is greatly influenced by the shape and deformability of RBCs, which can be affected by oxidative stress induced by different drugs and diseases leading to anemia. Here we investigated how in vitro microfluidic characterization of RBCs transit velocity in microcapillaries can indicate cells damage and its correlation with clinical hematological analysis. For this purpose, we compared an SU-8 mold with an Si-etched mold for fabrication of PDMS microfluidic devices and quantitatively figured out that oxidative stress induced by tert-Butyl hydroperoxide splits all RBCs into two subpopulations of normal and slow cells according to their transit velocity. Obtained results agree with the hematological analysis showing that such changes in RBCs velocities are due to violations of shape, volume, and increased heterogeneity of the cells. These data show that characterization of RBCs transport in microfluidic devices can directly reveal violations of microcirculation caused by oxidative stress. Therefore, it can be used for characterization of the ability of RBCs to move in microcapillaries, estimating possible side effects of cancer chemotherapy, and predicting the risk of anemia.

Melatonin chelates iron and binds directly with phenylhydrazine to provide protection against phenylhydrazine induced oxidative damage in red blood cells along with its antioxidant mechanisms: an in vitro study

2018 ◽  
Vol 1 (1) ◽  
pp. 1-20 ◽  
Author(s):  
Sudeshna Paul ◽  
Shamreen Naaz ◽  
Arnab Kumar Ghosh ◽  
Sanatan Mishra ◽  
Aindrila Chattopadhyay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Molecular Mechanisms ◽  
Radical Scavenging ◽  
In Vitro Study ◽  
Causative Factor ◽  
Protective Effects

Oxidative stress is an important causative factor for a number of diseases. Phenylhydrazine (PHZ) is a widely accepted model for studying hemolytic anemia by induction of oxidative stress. In the present study, goat red blood cells (RBCs) were incubated in vitro with PHZ (1mM) to generate oxidative stress. To test whether melatonin exhibits protective effects on PHZ induced RBC damage and to explore its potential molecular mechanisms, different concentrations of melatonin (5, 10, 20 and 40 nmoles/ml) were also included. PHZ caused altered profiles on biomarkers of oxidative stress and antioxidative as well as glucose metabolic enzymes in RBCs. These alterations indicated a development of oxidative stress. Melatonin at a concentration of 40 nmoles/ml provided optimal protection against all alterations induced by PHZ. The important cellular membrane proteins, including spectrin and actin, were also damaged by PHZ and this led to RBC deformation similar to that of observed in severe β-thalassaemia; the RBC deformation was also prevented by melatonin. Binding profiles of melatonin with PHZ and ferrous iron indicated favorable binding of melatonin with both of them, respectively. Thus, in addition to the direct antioxidant and free radical scavenging capability, melatonin also inhibited iron overloading by chelating iron and binding with the PHZ. This action of melatonin further reduces free radical generation. Based on the results, melatonin may provide therapeutic relevance to ß-thalassemia and other hemolytic RBC disorders involving oxidative stress. 

Melatonin Ameliorates BPA Induced Oxidative Stress in Human Red Blood Cells: An In vitro Study

2020 ◽  
Vol 20 (8) ◽  
pp. 1321-1327
Author(s):  
Saleh M. Abdullah ◽  
Hina Rashid
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Red Blood Cells ◽  
Blood Cells ◽  
In Vitro Study ◽  
Limited Data ◽  
Human Red Blood Cells ◽  
Living Organisms ◽  
Human Rbcs

Background: Bisphenol A (BPA) is a xenobiotic that causes oxidative stress in various organs in living organisms. Blood cells are also an endpoint where BPA is known to cause oxidative stress. Blood cells, especially red blood cells (RBCs), are crucial for maintaining homeostasis and overall wellbeing of the organism. They are highly susceptible to oxidative stress induced by xenobiotics. However, there is limited data about the oxidative stress induced by BPA in blood, especially in red blood cells. This study was carried out to evaluate BPA induced oxidative stress in human RBCs in vitro and its amelioration by melatonin. Objective: To find if melatonin exerts a protective effect on the oxidative stress induced by the BPA in human red blood cells in vitro. Methods: The erythrocyte suspensions (2 ml) were divided into six groups and treated with 0, 50, 100, 150, 200, and 250 μg/ml of BPA. Another set of erythrocyte suspension with similar BPA treatment and 50 μM Melatonin per group was also set. Incubations lasted for 12 hrs in the dark. Lipid peroxidation, glutathione, glutathione reductase, catalase, and superoxide dismutase were measured as indicators of oxidative stress. Results: BPA caused a significant increase in lipid peroxidation. A decrease in GSH levels was also observed. The activities of all the studied antioxidants also decreased with BPA treatment. Melatonin was seen to mitigate the oxidative stress induced by BPA. Conclusion: Treatment of red blood cells with BPA caused an increase in oxidative stress, while melatonin decreased the induced oxidative stress.

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