Nitric oxide ameliorates the damaging effects of oxidative stress induced by iron deficiency in cyanobacterium Anabaena 7120

2016 ◽  
Vol 23 (21) ◽  
pp. 21805-21821 ◽  
Author(s):  
Manish Singh Kaushik ◽  
Meenakshi Srivastava ◽  
Alka Srivastava ◽  
Anumeha Singh ◽  
Arun Kumar Mishra
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Iron Deficiency ◽  
Anabaena 7120 ◽  
Cyanobacterium Anabaena ◽  
Damaging Effects

scholarly journals Long-term Effect of Intravenous Iron Carboxymaltose Treatment on Oxidative Stress in Women with Iron Deficiency Anemia

2021 ◽  
pp. 3-10
Author(s):  
Gökhan Pektaş ◽  
İsmail Kırlı
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Catalase Activity ◽  
Intravenous Iron ◽  
Deficiency Anemia ◽  
Healthy Controls ◽  
Iron Treatment ◽  
Oxidant Status

Objective: This study aims to clarify the effects of intravenous iron supplementation on biomarkers for oxidative stress in women with iron deficiency anemia. Methods: This is a cross-sectional review of 40 healthy women and 40 women who underwent intravenous iron treatment due to anemia. Biochemical markers for oxidative stress were determined for both healthy controls and anemic patients. These markers were also evaluated at hour 1 and day 30 of intravenous iron treatment. Results: The patients with anemia had significantly higher catalase activity and total oxidant status (TOS) but significantly lower nitrate and total anti-oxidant status (TAS) than the healthy controls (p=0.0245, p<0.0001, p=0.0437 and p<0.0001 respectively). At hour 1 of intravenous iron treatment, nitrate, nitrite, nitric oxide, total thiol and TAS values were significantly lower and TOS values were significantly higher than those before the administration of treatment (p=0.0322, p=0.0003, p=0.0005, p<0.0001, p<0.0001 and p=0.004). At day 30 of intravenous iron treatment, catalase activity, nitrate, total thiol and TOS values were significantly lower than those before the administration of treatment (p=0.0332, p=0.0015, p=0.0391 and p<0.0001 respectively) and at hour 1 of treatment (p=0.0498, p<0.0001, p=0.0004 and p<0.0001 respectively). At day 30 of intravenous iron treatment, nitric oxide and TAS values were significantly higher than those before the administration of treatment (p=0.0480 and p=0.001 respectively) and at hour 1 of treatment (p<0.0001 for both). Conclusion: Intravenous iron replacement prompts oxidative stress at hour 1 of infusion in adults with anemia but this increase resolves partially in the following 30 days.

Protective effect of nitric oxide on iron deficiency-induced oxidative stress in maize (Zea mays)

2007 ◽  
Vol 164 (5) ◽  
pp. 536-543 ◽  
Author(s):  
Baoteng Sun ◽  
Yan Jing ◽  
Kunming Chen ◽  
Lili Song ◽  
Fangjian Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Zea Mays ◽  
Iron Deficiency ◽  
Protective Effect

scholarly journals Nitric oxide and oxidative stress (H2O2) control mammalian iron metabolism by different pathways.

1996 ◽  
Vol 16 (7) ◽  
pp. 3781-3788 ◽  
Author(s):  
K Pantopoulos ◽  
G Weiss ◽  
M W Hentze
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Iron Deficiency ◽  
Iron Metabolism ◽  
De Novo ◽  
Reactive Oxygen ◽  
Target Cells ◽  
Induction Phase ◽  
Reactive Oxygen Intermediate ◽  
Oxygen Intermediates

Several cellular mRNAs are regulated posttranscriptionally by iron-responsive elements (IREs) and the cytosolic IRE-binding proteins IRP-1 and IRP-2. Three different signals are known to elicit IRP-1 activity and thus regulate IRE-containing mRNAs: iron deficiency, nitric oxide (NO), and the reactive oxygen intermediate hydrogen peroxide (H2O2). In this report, we characterize the pathways for IRP-1 regulation by NO and H2O2 and examine their effects on IRP-2. We show that the responses of IRP-1 and IRP-2 to NO remarkably resemble those elicited by iron deficiency: IRP-1 induction by NO and by iron deficiency is slow and posttranslational, while IRP-2 induction by these inductive signals is slow and requires de novo protein synthesis. In contrast, H2O2 induces a rapid posttranslational activation which is limited to IRP-1. Removal of the inductive signal H2O2 after < or = 15 min of treatment (induction phase) permits a complete IRP-1 activation within 60 min (execution phase) which is sustained for several hours. This contrasts with the IRP-1 activation pathway by NO and iron depletion, in which NO-releasing drugs or iron chelators need to be present during the entire activation phase. Finally, we demonstrate that biologically synthesized NO regulates the expression of IRE-containing mRNAs in target cells by passive diffusion and that oxidative stress endogenously generated by pharmacological modulation of the mitochondrial respiratory chain activates IRP-1, underscoring the physiological significance of NO and reactive oxygen intermediates as regulators of cellular iron metabolism. We discuss models to explain the activation pathways of IRP-1 and IRP-2. In particular, we suggest the possibility that NO affects iron availability rather than the iron-sulfur cluster of IRP-1.

Astaxanthin, the Natural Antioxidant, Reduces Reserpine Induced Depression in Mice

2020 ◽  
Vol 16 (9) ◽  
pp. 1319-1327
Author(s):  
Ferdous Khan ◽  
Syed A. Kuddus ◽  
Md. H. Shohag ◽  
Hasan M. Reza ◽  
Murad Hossain
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reduced Glutathione ◽  
Forced Swim Test ◽  
Tail Suspension Test ◽  
Glutathione Depletion ◽  
Swim Test ◽  
Stress Markers ◽  
Immobility Time ◽  
Biochemical Level

Background: An imbalance between pro-oxidants and antioxidants determines the level of oxidative stress which is implicated in the etiopathogenesis of various neuropsychiatric disorders including depression. Therefore, treatment with antioxidants could potentially improve the balance between pro-oxidants and antioxidants. Objective: The objective of this study was to evaluate the ability of astaxanthin, a potential antioxidant, to reduce reserpine-induced depression in BALB/c mice (Mus musculus). Methods: On the behavioral level, antidepressant property of astaxanthin (50 mg/kg, orally) on reserpine (2 mg/kg, subcutaneously) induced depressed mice was evaluated by Forced Swim Test (FST) and Tail Suspension Test (TST). In the biochemical level, the ability of astaxanthin to mitigate reserpine-induced oxidative stress was evaluated by the measurement of Malondialdehyde (MDA) and nitric oxide (NO) in brain, liver and plasma samples. On the other hand, the efficiency of astaxanthin to replenish glutathione depletion and antioxidant enzyme activity augmentation in the same samples were also investigated. Results: Astaxanthin was able to lower reserpine induced immobility time significantly (p<0.05) in FST and TST. Mice treated with astaxanthin showed significantly (p<0.05) low level of oxidative stress markers such as Malondialdehyde (MDA), Nitric Oxide (NO). Consistently, the level of reduced Glutathione (GSH), and the activity of Superoxide Dismutase (SOD) and catalase were augmented due to the oral administration of astaxanthin. Conclusion: This study suggests that astaxanthin reduces reserpine-induced oxidative stress and therefore might be effective in treating oxidative stress associated depression.

Increased Production of Nitric Oxide Mediates Selective Organ-Specific Effects of Endotoxin on Oxidative Stress

2012 ◽  
Vol 11 (2) ◽  
pp. 161-172 ◽  
Author(s):  
Seyhan Sahan-Firat ◽  
Necmiye Canacankatan ◽  
Belma Korkmaz ◽  
Hatice Yildirim ◽  
Lulufer Tamer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Specific Effects ◽  
Organ Specific

scholarly journals Tetrahydrocurcumin alleviates hypertension, aortic stiffening and oxidative stress in rats with nitric oxide deficiency

2011 ◽  
Vol 35 (4) ◽  
pp. 418-425 ◽  
Author(s):  
Saowanee Nakmareong ◽  
Upa Kukongviriyapan ◽  
Poungrat Pakdeechote ◽  
Veerapol Kukongviriyapan ◽  
Bunkerd Kongyingyoes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Deficiency ◽  
Aortic Stiffening ◽  
And Oxidative Stress

scholarly journals Effect of Shuangdan Mingmu capsule, a Chinese herbal formula, on oxidative stress-induced apoptosis of pericytes through PARP/GAPDH pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Fujiao Nie ◽  
Jiazhao Yan ◽  
Yanjun Ling ◽  
Zhengrong Liu ◽  
Chaojun Fu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Oxidative Damage ◽  
Damage Model ◽  
B Cell Lymphoma ◽  
Cell Counting ◽  
Network Pharmacology ◽  
Diabetic Patients ◽  
Induced Apoptosis

Abstract Background Diabetic retinopathy (DR) has become a worldwide concern because of the rising prevalence rate of diabetes mellitus (DM). Despite much energy has been committed to DR research, it remains a difficulty for diabetic patients all over the world. Since apoptosis of retinal microvascular pericytes (RMPs) is the early characteristic of DR, this study aimed to reveal the mechanism of Shuangdan Mingmu (SDMM) capsule, a Chinese patent medicine, on oxidative stress-induced apoptosis of pericytes implicated with poly (ADP-ribose) polymerase (PARP) / glyceraldehyde 3-phosphate dehydrogenase (GAPDH) pathway. Methods Network pharmacology approach was performed to predict biofunction of components of SDMM capsule dissolved in plasma on DR. Both PARP1 and GAPDH were found involved in the hub network of protein-protein interaction (PPI) of potential targets and were found to take part in many bioprocesses, including responding to the regulation of reactive oxygen species (ROS) metabolic process, apoptotic signaling pathway, and response to oxygen levels through enrichment analysis. Therefore, in vitro research was carried out to validate the prediction. Human RMPs cultured with media containing 0.5 mM hydrogen oxide (H2O2) for 4 h was performed as an oxidative-damage model. Different concentrations of SDMM capsule, PARP1 inhibitor, PARP1 activation, and GAPDH inhibitor were used to intervene the oxidative-damage model with N-Acetyl-L-cysteine (NAC) as a contrast. Flow cytometry was performed to determine the apoptosis rate of cells and the expression of ROS. Cell counting kit 8 (CCK8) was used to determine the activity of pericytes. Moreover, nitric oxide (NO) concentration of cells supernatant and expression of endothelial nitric oxide synthase (eNOS), superoxide dismutase (SOD), B cell lymphoma 2 (BCL2), vascular endothelial growth factor (VEGF), endothelin 1 (ET1), PARP1, and GAPDH were tested through RT-qPCR, western blot (WB), or immunocytochemistry (ICC). Results Overproduction of ROS, high apoptotic rate, and attenuated activity of pericytes were observed after cells were incubated with media containing 0.5 mM H2O2. Moreover, downregulation of SOD, NO, BCL2, and GAPDH, and upregulation of VEGFA, ET1, and PARP1 were discovered after cells were exposed to 0.5 mM H2O2 in this study, which could be improved by PARP1 inhibitor and SDMM capsule in a dose-dependent way, whereas worsened by PARP1 activation and GAPDH inhibitor. Conclusions SDMM capsule may attenuate oxidative stress-induced apoptosis of pericytes through downregulating PARP expression and upregulating GAPDH expression.

scholarly journals Melatonin and Microglia

2021 ◽  
Vol 22 (15) ◽  
pp. 8296
Author(s):  
Rüdiger Hardeland
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Signal Transduction ◽  
Endothelial Cells ◽  
Bacterial Infections ◽  
Melatonin Receptors ◽  
Sterile Inflammation ◽  
High Complexity ◽  
Anti Inflammatory ◽  
Multiple Signaling

Melatonin interacts in multiple ways with microglia, both directly and, via routes of crosstalk with astrocytes and neurons, indirectly. These effects of melatonin are of relevance in terms of antioxidative protection, not only concerning free-radical detoxification, but also in prevention of processes that cause, promote, or propagate oxidative stress and neurodegeneration, such as overexcitation, toxicological insults, viral and bacterial infections, and sterile inflammation of different grades. The immunological interplay in the CNS, with microglia playing a central role, is of high complexity and includes signaling toward endothelial cells and other leukocytes by cytokines, chemokines, nitric oxide, and eikosanoids. Melatonin interferes with these processes in multiple signaling routes and steps. In addition to canonical signal transduction by MT1 and MT2 melatonin receptors, secondary and tertiary signaling is of relevance and has to be considered, e.g., via the upregulation of sirtuins and the modulation of pro- and anti-inflammatory microRNAs. Many details concerning the modulation of macrophage functionality by melatonin are obviously also applicable to microglial cells. Of particular interest is the polarization toward M2 subtypes instead of M1, i.e., in favor of being anti-inflammatory at the expense of proinflammatory activities, which is well-documented in macrophages but also applies to microglia.

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