scholarly journals DETEKSI CEKAMAN OKSIDATIF AKIBAT TOKSISITAS KROM PADASonchus oleraceus L. MELALUI PENENTUAN SPESIES OKSIGEN REAKTIF SECARA SPEKTROFOTOMETRI DAN HISTOKIMIA

Agric ◽  
2016 ◽  
Vol 26 (1) ◽  
pp. 85
Author(s):  
Sri Kasmiyati ◽  
Sucahyo
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Ros Generation ◽  
Toxic Heavy Metal ◽  
Sonchus Oleraceus ◽  
Wide Range ◽  
Weed Plants ◽  
Antioxidant Defense Systems ◽  
Textile Sludge ◽  
Endogenous Antioxidant

<p>Increased production of reactive oxygen species or ROS is one of the common responses to a wide range of biotic and abiotic stresses. Increased production of ROS is outstripping endogenous antioxidant defense systems has been referred to as oxidative stress. Heavy metals are known to initiate ROS generation which is implicated as a oxidative stress. Cr is a toxic heavy metal that can generate ROS like H2O2 and O2 - which cause oxidative stress. In this study, chromium toxicity was studied to detect the oxidative stress on Sonchus oleraceus weed plants by the detection of superoxide anion and H2O2. Superoxide anion was detected by staining techniques with nitroblue tetrazolium (NBT) and hydrogen peroxide by Diaminobenzidine tetrahydrochloride (DAB) staining. Results indicated that the plants were grown in sand media generate the highest (0.89 A/g FW and 3.23 mol/g FW) than in soil media (0.23 A/g FW and 2.11 mol/g FW) superoxide anion (*O- 2) and H2O2 and soil containing textile sludge (0.18 A/g FW and 2.66 mol/g FW), respectively. At application of 10 mg Cr6+/L and 250 mg Cr3+/L, the production of *O- 2 and H2O2 in leaves of sonchus plants were significantly increased compared with the control plants. The highest production of H2O2 and *O- 2 were showed in the leaves of sonchus plants grown in sand media with Cr6+ application. In this study, either Cr3+ or Cr6+ caused oxidative stress in Sonchus oleraceus weed plants. The result also showed that sonchus plants esposed to toxic Cr can suffer from oxidative stress leading to reduction of its fresh and dry plants biomass. NBT and DAB in an appropriate probe and significant value for monitoring the formation of *O- 2 and H2O2 in plants.</p>

scholarly journals Oxygen Is Instrumental for Biological Signaling: An Overview

Oxygen ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 3-15
Author(s):  
John T. Hancock
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Nitrosative Stress ◽  
Redox Status ◽  
Complex Interplay ◽  
Wide Range ◽  
Form Part ◽  
High Concentrations ◽  
And Control ◽  
Signaling Components

Control of cellular function is extremely complex, being reliant on a wide range of components. Several of these are small oxygen-based molecules. Although reactive compounds containing oxygen are usually harmful to cells when accumulated to relatively high concentrations, they are also instrumental in the control of the activity of a myriad of proteins, and control both the upregulation and downregulation of gene expression. The formation of one oxygen-based molecule, such as the superoxide anion, can lead to a cascade of downstream generation of others, such as hydrogen peroxide (H2O2) and the hydroxyl radical (∙OH), each with their own reactivity and effect. Nitrogen-based signaling molecules also contain oxygen, and include nitric oxide (NO) and peroxynitrite, both instrumental among the suite of cell signaling components. These molecules do not act alone, but form part of a complex interplay of reactions, including with several sulfur-based compounds, such as glutathione and hydrogen sulfide (H2S). Overaccumulation of oxygen-based reactive compounds may alter the redox status of the cell and lead to programmed cell death, in processes referred to as oxidative stress, or nitrosative stress (for nitrogen-based molecules). Here, an overview of the main oxygen-based molecules involved, and the ramifications of their production, is given.

scholarly journals Protective Effects of Aqueous Extract of Mentha suaveolens against Oxidative Stress-Induced Damages in Human Keratinocyte HaCaT Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
HansongI Lee ◽  
Miji Yeom ◽  
Seoungwoo Shin ◽  
Kyungeun Jeon ◽  
Deokhoon Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Phase Ii ◽  
Aqueous Extract ◽  
Biological Activities ◽  
Ros Generation ◽  
Related Factor ◽  
Hacat Cells ◽  
Human Keratinocyte ◽  
Wide Range ◽  
Phase Ii Enzyme

Mentha suaveolens is an aromatic herb that has a wide range of biological activities, including antimicrobial, antifungal, anti-inflammatory, and hepatoprotective properties. Although there are a few reports on the antioxidant property of M. suaveolens, its cytoprotective activity against oxidative stress has not been reported yet. The objective of this study was to determine the protective activity of M. suaveolens aqueous extract (MSAE) against hydrogen peroxide- (H2O2-) induced oxidative stress and apoptosis in human keratinocyte HaCaT cells. MSAE pretreatment decreased H2O2-induced cytotoxicity and suppressed H2O2-induced intracellular ROS generation. Furthermore, MSAE suppressed expression levels of H2O2-induced apoptotic genes such as cleaved caspase-3, caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP). Pretreatment with MSAE induced expression of phase II enzyme such as HO-1 through translocation of NF-E2-related factor (Nrf2) upon H2O2 exposure. These results revealed that the cytoprotective effect of MSAE against oxidative stress-induced cell death was associated with activation of Nrf2-mediated phase II enzyme expression.

scholarly journals Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics

2015 ◽  
Vol 36 (3) ◽  
pp. 966-979 ◽  
Author(s):  
Hao Liu ◽  
Ping Mao ◽  
Jia Wang ◽  
Tuo Wang ◽  
Chang-Hou Xie
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Pc12 Cells ◽  
Atp Synthesis ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Cytochrome C Release ◽  
Endogenous Antioxidant

Background: Parkinson disease (PD) is a common adult-onset neurodegenerative disorder, and PD related neuronal injury is associated with oxidative stress and mitochondrial dysfunction. Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies. Methods: The present study aimed to investigate the potential protective role of allicin in an in vitro PD model induced by 6-hydroxydopamine (6-OHDA) in PC12 cells. The protective effects were measured by cell viability, decreased lactate dehydrogenase (LDH) release and flow cytometry, and the anti-oxidative activity was determined by reactive oxygen species (ROS) generation, lipid peroxidation and the endogenous antioxidant enzyme activities. Mitochondrial function in PC12 cells was detected by mitochondrial membrane potential (MMP) collapse, cytochrome c release, mitochondrial ATP synthesis, and the mitochondrial Ca2+ buffering capacity. To investigate the potential mechanism, we also measured the expression of mitochondrial biogenesis factors, mitochondrial morphological dynamic changes, as well as detected mitochondrial dynamic proteins by western blot. Results: We found that allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure. Allicin also inhibited ROS generation, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities. These protective effects were associated with suppressed mitochondrial dysfunction, as evidenced by decreased MMP collapse and cytochrome c release, preserved mitochondrial ATP synthesis, and the promotion of mitochondrial Ca2+ buffering capacity. In addition, allicin significantly enhanced mitochondrial biogenesis and prevented fragmentation of mitochondrial network after 6-OHDA treatment. The results of western blot analysis showed that the 6-OHDA induced decrease in the expression of optic atrophy type 1 (Opa-1), increase in mitochondrial fission 1 (Fis-1) and dynamin-related protein 1 (Drp-1) were all partially revised by allicin. Conclusion: In summary, our data strongly suggested that allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

scholarly journals Neuroprotective Effects of Cornus officinalis on Stress-Induced Hippocampal Deficits in Rats and H2O2-Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 27 ◽  
Author(s):  
Weishun Tian ◽  
Jing Zhao ◽  
Jeong-Ho Lee ◽  
Md Rashedunnabi Akanda ◽  
Jeong-Hwi Cho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Forced Swim Test ◽  
Neuroblastoma Cells ◽  
Mitogen Activated Protein Kinase ◽  
Ros Generation ◽  
Neuroprotective Effects ◽  
Neuronal Markers ◽  
Cornus Officinalis ◽  
Immobility Time ◽  
Wide Range

Oxidative stress plays a vital role in neurodegenerative diseases. Cornus officinalis (CC) has a wide range of pharmacological activities (e.g., antioxidant, neuroprotective, and anti-inflammatory). The present study was undertaken to elucidate the neuroprotective mechanism of CC and fermented CC (FCC) on stress and H2O2-induced oxidative stress damage in rats and SH-SY5Y cells. A dose of 100 mg/kg CC or FCC was orally administered to rats 1 h prior to immobilization 2 h per day for 14 days. CC, especially FCC administration decreased immobility time in forced swim test (FST), effectively alleviated the oxidative stress, and remarkably decreased corticosterone, β-endorphin and increased serotonin levels, respectively. In cells, CC and FCC significantly inhibited reactive oxygen species (ROS) generation, lactate dehydrogenase (LDH) release and significantly increased the genes expression of antioxidant and neuronal markers, such as superoxide dismutase (SOD), catalase (CAT), and brain-derived neurotrophic factor (BDNF). Moreover, the pro-apoptotic factor Bax and anti-apoptotic factor Bcl-2 (Bax/Bcl-2) ratio was regulated by CC and FCC pretreatment. Both in rats and cells, CC and FCC downregulated mitogen-activated protein kinase (MAPK) phosphorylation. Taken together, these results demonstrated that CC and particularly FCC ameliorated oxidative stress and may be used on the neuroprotection.

Role of antioxidant activity of taurine in diabetesThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

2009 ◽  
Vol 87 (2) ◽  
pp. 91-99 ◽  
Author(s):  
Stephen W. Schaffer ◽  
Junichi Azuma ◽  
Mahmood Mozaffari
Keyword(s):  
Antioxidant Activity ◽  
Respiratory Chain ◽  
Superoxide Anion ◽  
Hypochlorous Acid ◽  
Antioxidant Defenses ◽  
Ros Generation ◽  
Superoxide Anion Production ◽  
Taurine Deficiency ◽  
Respiratory Chain Activity ◽  
Endogenous Antioxidant

The unifying hypothesis of diabetes maintains that reactive oxygen species (ROS) generated in the mitochondria of glucose-treated cells promote reactions leading to the development of diabetic complications. Although the unifying hypothesis attributes the generation of oxidants solely to impaired glucose and fatty acid metabolism, diabetes is also associated with a decline in the levels of the endogenous antioxidant taurine in a number of tissues, raising the possibility that changes in taurine status might also contribute to the severity of oxidant-mediated damage. There is overwhelming evidence that taurine blocks toxicity caused by oxidative stress, but the mechanism underlying the antioxidant activity remains unclear. One established antioxidant action of taurine is the detoxification of hypochlorous acid. However, not all of the antioxidant actions of taurine are related to hypochlorous acid because they are detected in isolated cell systems lacking neutrophils. There are a few studies showing that taurine either modulates the antioxidant defenses or blocks the actions of the oxidants, but other studies oppose this interpretation. Although taurine is incapable of directly scavenging the classic ROS, such as superoxide anion, hydroxyl radical, and hydrogen peroxide, there are numerous studies suggesting that it is an effective inhibitor of ROS generation. The present review introduces a novel antioxidant hypothesis, which takes into consideration the presence of taurine-conjugated tRNAs in the mitochondria. Because tRNA conjugation is required for normal translation of mitochondrial-encoded proteins, taurine deficiency reduces the expression of these respiratory chain components. As a result, flux through the electron transport chain decreases. The dysfunctional respiratory chain accumulates electron donors, which divert electrons from the respiratory chain to oxygen, forming superoxide anion in the process. Restoration of taurine levels increases the levels of conjugated tRNA, restores respiratory chain activity, and increases the synthesis of ATP at the expense of superoxide anion production. The importance of this and other actions of taurine in diabetes is discussed.

scholarly journals Astragaloside IV Attenuates Myocardial Ischemia-Reperfusion Injury from Oxidative Stress by Regulating Succinate, Lysophospholipid Metabolism, and ROS Scavenging System

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Miaomiao Jiang ◽  
Jingyu Ni ◽  
Yuanlin Cao ◽  
Xiaoxue Xing ◽  
Qian Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Ros Generation ◽  
Heme Oxygenase 1 ◽  
Ros Scavenging ◽  
Astragaloside Iv ◽  
Wide Range

Astragaloside IV is one of the main active ingredients isolated from Astragalus membranaceus. Here we confirmed its protective effect against cardiac ischemia-reperfusion (I/R) injury and aimed to investigate the potential molecular mechanisms involved. Pretreatment of ex vivo and in vivo I/R-induced rat models by astragaloside IV significantly prevented the ratio of myocardium infarct size, systolic and diastolic dysfunction, and the production of creatine kinase and lactate dehydrogenase. Metabolic analyses showed that I/R injury caused a notable reduction of succinate and elevation of lysophospholipids, indicating excessive reactive oxygen species (ROS) generation driven by succinate’s rapid reoxidization and glycerophospholipid degradation. Molecular validation mechanistically revealed that astragaloside IV stimulated nuclear factor (erythroid-derived 2)-like 2 (Nrf2) released from Kelch-like ECH-associated protein 1 (Keap1) and translocated to the nucleus to combine with musculoaponeurotic fibrosarcoma (Maf) to initiate the transcription of antioxidative gene heme oxygenase-1 (HO-1), which performed a wide range of ROS scavenging processes against pathological oxidative stress in the hearts. As expected, increasing succinate and decreasing lysophospholipid levels were observed in the astragaloside IV-pretreated group compared with the I/R model group. These results suggested that astragaloside IV ameliorated myocardial I/R injury by modulating succinate and lysophospholipid metabolism and scavenging ROS via the Nrf2 signal pathway.

scholarly journals Oxidative Stress and Vascular Damage in Hypertension: Role of Angiotensin II

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Agostino Virdis ◽  
Emiliano Duranti ◽  
Stefano Taddei
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Active Role ◽  
Vascular Wall ◽  
Ros Generation ◽  
Low Concentrations ◽  
Endogenous Antioxidant ◽  
And Function ◽  
Antioxidant Mechanisms

Reactive oxygen species are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. In healthy conditions, ROS are produced in a controlled manner at low concentrations and function as signaling molecules regulating vascular contraction-relaxation and cell growth. Physiologically, the rate of ROS generation is counterbalanced by the rate of elimination. In hypertension, an enhanced ROS generation occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. In the present paper, major angiotensin II-induced vascular ROS generation within the vasculature, and relative sources, will be discussed. Recent development of signalling pathways whereby angiotensin II-driven vascular ROS induce and accelerate functional and structural vascular injury will be also considered.

scholarly journals Oxidative status in plasma, urine and saliva of girls with anorexia nervosa and healthy controls: a cross-sectional study

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Alexandra Gaál Kovalčíková ◽  
Ľubica Tichá ◽  
Katarína Šebeková ◽  
Peter Celec ◽  
Alžbeta Čagalová ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Anorexia Nervosa ◽  
Redox Homeostasis ◽  
Oxidative Status ◽  
Carbonyl Stress ◽  
Healthy Controls ◽  
Psychosomatic Disorder ◽  
Cross Sectional ◽  
Wide Range ◽  
Markers Of Oxidative Stress

Abstract Background Anorexia nervosa (AN) is a serious psychosomatic disorder with unclear pathomechanisms. Metabolic dysregulation is associated with disruption of redox homeostasis that might play a pivotal role in the development of AN. The aim of our study was to assess oxidative status and carbonyl stress in plasma, urine and saliva of patients with AN and healthy controls. Methods Plasma, spot urine, and saliva were collected from 111 girls with AN (aged from 10 to 18 years) and from 29 age-matched controls. Markers of oxidative stress and antioxidant status were measured using spectrophotometric and fluorometric methods. Results Plasma advanced oxidation protein products (AOPP) and advanced glycation end products (AGEs) were significantly higher in patients with AN than in healthy controls (by 96, and 82%, respectively). Accordingly, urinary concentrations of AOPP and fructosamines and salivary concentrations of AGEs were higher in girls with AN compared with controls (by 250, and 41% in urine; by 92% in saliva, respectively). Concentrations of thiobarbituric acid reactive substances (TBARS) in saliva were 3-times higher in the patients with AN than in the controls. Overall antioxidants were lower in plasma of girls with AN compared to the controls, as shown by total antioxidant capacity and ratio of reduced and oxidized glutathione (by 43, and 31%, respectively). Conclusions This is the first study assessing wide range of markers of oxidative status in plasma, urine and saliva of the patients with AN. We showed that both, higher levels of markers of oxidative stress and lower antioxidants play a role in redox disruption. Restoration of redox homeostasis might be of the clinical relevance

scholarly journals The Use of Coenzyme Q10 in Cardiovascular Diseases

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 755
Author(s):  
Yoana Rabanal-Ruiz ◽  
Emilio Llanos-González ◽  
Francisco J. Alcain
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Vascular System ◽  
Contractile Function ◽  
Artery Bypass ◽  
Bypass Graft ◽  
No Bioavailability ◽  
Coq10 Supplementation ◽  
Endogenous Antioxidant

CoQ10 is an endogenous antioxidant produced in all cells that plays an essential role in energy metabolism and antioxidant protection. CoQ10 distribution is not uniform among different organs, and the highest concentration is observed in the heart, though its levels decrease with age. Advanced age is the major risk factor for cardiovascular disease and endothelial dysfunction triggered by oxidative stress that impairs mitochondrial bioenergetic and reduces NO bioavailability, thus affecting vasodilatation. The rationale of the use of CoQ10 in cardiovascular diseases is that the loss of contractile function due to an energy depletion status in the mitochondria and reduced levels of NO for vasodilatation has been associated with low endogenous CoQ10 levels. Clinical evidence shows that CoQ10 supplementation for prolonged periods is safe, well-tolerated and significantly increases the concentration of CoQ10 in plasma up to 3–5 µg/mL. CoQ10 supplementation reduces oxidative stress and mortality from cardiovascular causes and improves clinical outcome in patients undergoing coronary artery bypass graft surgery, prevents the accumulation of oxLDL in arteries, decreases vascular stiffness and hypertension, improves endothelial dysfunction by reducing the source of ROS in the vascular system and increases the NO levels for vasodilation.

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