Corrigendum to: Peroxynitrite formation in nitric oxide-exposed submitochondrial particles: Detection, oxidative damage and catalytic removal by Mn–porphyrins [Arch. Biochem. Biophys. 529 (2013) 45–54]

2014 ◽  
Vol 547 ◽  
pp. 44
Author(s):  
Valeria Valez ◽  
Adriana Cassina ◽  
Ines Batinic-Haberle ◽  
Balaraman Kalyanaraman ◽  
Gerardo Ferrer-Sueta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxidative Damage ◽  
Submitochondrial Particles ◽  
Catalytic Removal ◽  
Mn Porphyrins

scholarly journals Peroxynitrite formation in nitric oxide-exposed submitochondrial particles: Detection, oxidative damage and catalytic removal by Mn–porphyrins

2013 ◽  
Vol 529 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Valeria Valez ◽  
Adriana Cassina ◽  
Ines Batinic-Haberle ◽  
Balaraman Kalyanaraman ◽  
Gerardo Ferrer-Sueta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxidative Damage ◽  
Submitochondrial Particles ◽  
Catalytic Removal ◽  
Mn Porphyrins

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 Role of Oxidative and Nitro-Oxidative Damage in Silver Nanoparticles Cytotoxic Effect against Human Pancreatic Ductal Adenocarcinoma Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Ewelina Barcińska ◽  
Justyna Wierzbicka ◽  
Agata Zauszkiewicz-Pawlak ◽  
Dagmara Jacewicz ◽  
Aleksandra Dabrowska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Pancreatic Cancer ◽  
Silver Nanoparticles ◽  
Oxidative Damage ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cytotoxic Effect ◽  
Mrna Level ◽  
Ductal Adenocarcinoma ◽  
Adenocarcinoma Cells

Pancreatic ductal adenocarcinoma is one of the most aggressive human malignancies, where the 5-year survival rate is less than 4% worldwide. Successful treatment of pancreatic cancer is a challenge for today’s oncology. Several studies showed that increased levels of oxidative stress may cause cancer cells damage and death. Therefore, we hypothesized that oxidative as well as nitro-oxidative stress is one of the mechanisms inducing pancreatic cancer programmed cell death. We decided to use silver nanoparticles (AgNPs) (2.6 and 18 nm) as a key factor triggering the reactive oxygen species (ROS) and reactive nitrogen species (RNS) in pancreatic ductal adenocarcinoma cells (PANC-1). Previously, we have found that AgNPs induced PANC-1 cells death. Furthermore, it is known that AgNPs may induce an accumulation of ROS and alteration of antioxidant systems in different type of tumors, and they are indicated as promising agents for cancer therapy. Then, the aim of our study was to evaluate the implication of oxidative and nitro-oxidative stress in this cytotoxic effect of AgNPs against PANC-1 cells. We determined AgNP-induced increase of ROS level in PANC-1 cells and pancreatic noncancer cell (hTERT-HPNE) for comparison purposes. We found that the increase was lower in noncancer cells. Reduction of mitochondrial membrane potential and changes in the cell cycle were also observed. Additionally, we determined the increase in RNS level: nitric oxide (NO) and nitric dioxide (NO2) in PANC-1 cells, together with increase in family of nitric oxide synthases (iNOS, eNOS, and nNOS) at protein and mRNA level. Disturbance of antioxidant enzymes: superoxide dismutase (SOD1, SOD2, and SOD3), glutathione peroxidase (GPX-4) and catalase (CAT) were proved at protein and mRNA level. Moreover, we showed cells ultrastructural changes, characteristic for oxidative damage. Summarizing, oxidative and nitro-oxidative stress and mitochondrial disruption are implicated in AgNPs-mediated death in human pancreatic ductal adenocarcinoma cells.

scholarly journals Nitric oxide synthase-mediated early nitric oxide burst alleviates water stress-induced oxidative damage in ammonium-supplied rice roots

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiaochuang Cao ◽  
Chunquan Zhu ◽  
Chu Zhong ◽  
Junhua Zhang ◽  
Lianghuan Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Water Stress ◽  
Nitric Oxide Synthase ◽  
Oxidative Damage ◽  
Rice Roots ◽  
Oxide Synthase

Activity of nitric oxide synthase isoforms in acute brain oxidative damage induced by ozone exposure

Nitric Oxide ◽  
2018 ◽  
Vol 75 ◽  
pp. 42-52 ◽  
Author(s):  
Juan Carlos Martínez-Lazcano ◽  
Edith González-Guevara ◽  
Verónica Custodio ◽  
Francisca Pérez-Severiano ◽  
Karen Olvera-Pérez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxidative Damage ◽  
Ozone Exposure ◽  
Oxide Synthase

scholarly journals Protective Effect of Nitric Oxide (NO) against Oxidative Damage in Larix gmelinii Seedlings under Ultraviolet-B Irradiation

Forests ◽  
2016 ◽  
Vol 7 (12) ◽  
pp. 251 ◽  
Author(s):  
Haiqing Hu ◽  
Zhenbao Zhou ◽  
Xiaoxin Sun ◽  
Zhonghua Zhang ◽  
Qinghuan Meng
Keyword(s):  
Nitric Oxide ◽  
Oxidative Damage ◽  
Protective Effect ◽  
Ultraviolet B ◽  
Larix Gmelinii ◽  
Ultraviolet B Irradiation

Nitric oxide alleviates oxidative damage in the green algaChlorella pyrenoidosa caused by UV-B radiation

2003 ◽  
Vol 48 (3) ◽  
pp. 389-393 ◽  
Author(s):  
K. Chen ◽  
H. Feng ◽  
M. Zhang ◽  
X. Wang
Keyword(s):  
Nitric Oxide ◽  
Oxidative Damage

scholarly journals Placental Adaptive Changes to Protect Function and Decrease Oxidative Damage in Metabolically Healthy Maternal Obesity

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 794 ◽  
Author(s):  
Celeste Santos-Rosendo ◽  
Fernando Bugatto ◽  
Alvaro González-Domínguez ◽  
Alfonso M. Lechuga-Sancho ◽  
Rosa Maria Mateos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxidative Damage ◽  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Nitrosative Stress ◽  
Antioxidant Response ◽  
Placental Function ◽  
Total Antioxidant ◽  
Metabolically Healthy ◽  
Inducible Nitric Oxide

Pregnancy-related disorders, including preeclampsia and gestational diabetes, are characterized by the presence of an adverse intrauterine milieu that may ultimately result in oxidative and nitrosative stress. This scenario may trigger uncontrolled production of reactive oxygen species (ROS) such as superoxide anion (O●−) and reactive nitrogen species (RNS) such as nitric oxide (NO), along with an inactivation of antioxidant systems, which are associated with the occurrence of relevant changes in placental function through recognized redox post-translational modifications in key proteins. The general objective of this study was to assess the impact of a maternal obesogenic enviroment on the regulation of the placental nitroso-redox balance at the end of pregnancy. We measured oxidative damage markers—thiobarbituric acid-reacting substances (TBARS) and carbonyl groups (C=O) levels; nitrosative stress markers—inducible nitric oxide synthase, nitrosothiol groups, and nitrotyrosine residues levels; and the antioxidant biomarkers—catalase and superoxide dismutase (SOD) activity and expression, and total antioxidant capacity (TAC), in full-term placental villous from both pre-pregnancy normal weight and obese women, and with absence of metabolic complications throughout gestation. The results showed a decrease in C=O and TBARS levels in obese pregnancies. Although total SOD and catalase concentrations were shown to be increased, both activities were significantly downregulated in obese pregnancies, along with total antioxidant capacity. Inducible nitric oxide sintase levels were increased in the obese group compared to the lean group, accompanied by an increase in nitrotyrosine residues levels and lower levels of nitrosothiol groups in proteins such as ERK1/2. These findings reveal a reduction in oxidative damage, accompanied by a decline in antioxidant response, and an increase via NO-mediated nitrative stress in placental tissue from metabolically healthy pregnancies with obesity. All this plausibly points to a placental adaptation of the affected antioxidant response towards a NO-induced alternative pathway, through changes in the ROS/RNS balance, in order to reduce oxidative damage and preserve placental function in pregnancy.

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