scholarly journals Nitric oxide improves tolerance to arsenic stress in Isatis cappadocica desv. Shoots by enhancing antioxidant defenses

Chemosphere ◽  
2020 ◽  
Vol 239 ◽  
pp. 124523 ◽  
Author(s):  
Zahra Souri ◽  
Naser Karimi ◽  
Muhammad Ansar Farooq ◽  
Luisa M. Sandalio
Author(s):  
Lindsay Zilliox ◽  
James W. Russell

Impaired glucose regulation (IGR) constitutes a spectrum of impaired glucose and metabolic regulation that can result in neuropathy. Several different pathways of injury in the diabetic peripheral nervous system that include metabolic dysregulation induced by metabolic syndrome induce oxidative stress, failure of nitric oxide regulation, and dysfunction of certain key signaling pathways. Oxidative stress can directly injure both dorsal route ganglion neurons and axons. Modulation of the nitric oxide system may have detrimental effects on endothelial function and neuronal survival. Reactive oxidative species can alter mitochondrial function, protein and DNA structure, interfere with signaling pathways, and deplete antioxidant defenses. Advanced glycelation end (AGE) products and formation of ROS are activated by and in turn regulate key signal transduction pathways.


2007 ◽  
Vol 292 (5) ◽  
pp. C1569-C1580 ◽  
Author(s):  
Maria Cecilia Carreras ◽  
Juan José Poderoso

Mitochondria are the specialized organelles for energy metabolism, but, as a typical example of system biology, they also activate a multiplicity of pathways that modulate cell proliferation and mitochondrial biogenesis or oppositely promote cell arrest and programmed cell death by a limited number of oxidative or nitrosative reactions. These reactions are influenced by matrix nitric oxide (NO) steady-state concentration, either from local production or by gas diffusion to mitochondria from the canonical sources. Likewise, in a range of ∼30–200 nM, NO turns mitochondrial O2utilization down by binding to cytochrome oxidase and elicits a burst of superoxide anion and hydrogen peroxide that diffuses outside mitochondria. Depending on NO levels and antioxidant defenses, more or less H2O2accumulates in cytosol and nucleus, and the resulting redox grading contributes to dual activation of proliferating and proapoptotic cascades, like ERK1/2 or p38 MAPK. Moreover, these sequential activating pathways participate in rat liver and brain development and in thyroid modulation of mitochondrial metabolism and contribute to hypothyroid phenotype through complex I nitration. On the contrary, lack of NO disrupts pathways like S-nitrosylation or H2O2production and likewise is a gateway to disease in amyotrophic lateral sclerosis with superoxide dismutase 1 mutations or to cancer proliferation.


2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Ayman M. Mahmoud ◽  
Sultan Alqahtani ◽  
Sarah I. Othman ◽  
Mousa O. Germoush ◽  
Omnia E. Hussein ◽  
...  

Hyperammonemia is a serious complication of liver disease and may lead to encephalopathy and death. This study investigated the effects ofCommiphora molmolresin on oxidative stress, inflammation, and hematological alterations in ammonium chloride- (NH4Cl-) induced hyperammonemic rats, with an emphasis on the glutamate-NO-cGMP and Nrf2/ARE/HO-1 signaling pathways. Rats received NH4Cl andC. molmolfor 8 weeks. NH4Cl-induced rats showed significant increase in blood ammonia, liver function markers, and tumor necrosis factor-alpha (TNF-α). Concurrent supplementation ofC. molmolsignificantly decreased circulating ammonia, liver function markers, and TNF-αin hyperammonemic rats.C. molmolsuppressed lipid peroxidation and nitric oxide and enhanced the antioxidant defenses in the liver, kidney, and cerebrum of hyperammonemic rats.C. molmolsignificantly upregulated Nrf2 and HO-1 and decreased glutamine and nitric oxide synthase, soluble guanylate cyclase, and Na+/K+-ATPase expression in the cerebrum of NH4Cl-induced hyperammonemic rats. Hyperammonemia was also associated with hematological and coagulation system alterations. These alterations were reversed byC. molmol. Our findings demonstrated thatC. molmolattenuates ammonia-induced liver injury, oxidative stress, inflammation, and hematological alterations. This study points to the modulatory effect ofC. molmolon glutamate-NO-cGMP and Nrf2/ARE/HO-1 pathways in hyperammonemia. Therefore,C. molmolmight be a promising protective agent against hyperammonemia.


2018 ◽  
Author(s):  
Cao Xiaochuang ◽  
Zhu Chunquan ◽  
Zhong Chu ◽  
Zhang Junhua ◽  
Zhu Lianfeng ◽  
...  

AbstractAmmonium (NH4+) can enhance rice drought tolerance in comparison to nitrate (NO3-). The mechanism underpinning this relationship was investigated based on the time-dependent nitric oxide (NO) production and its protective role in oxidative stress of NH4+-/NO3--supplied rice under drought. An early burst of NO was induced by drought 3h after root NH4+ treatment but not after NO3- treatment. Root oxidative damage induced by drought was significantly higher in NO3- than in NH4+-treatment due to its reactive oxygen species accumulation. Inducing NO production by applying NO donor 3h after NO3- treatment alleviated the oxidative damage, while inhibiting the early NO burst increased root oxidative damage in NH4+ treatment. Application of nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) completely suppressed NO synthesis in roots 3h after NH4+ treatment and aggravated drought-induced oxidative damage, indicating the aggravation of oxidative damage might have resulted from changes in NOS-mediated early NO burst. Drought also increased root antioxidant enzymes activities, which were further induced by NO donor but repressed by NO scavenger and NOS inhibitor in NH4+-treated roots. Thus, the NOS-mediated early NO burst plays an important role in alleviating oxidative damage induced by drought by enhancing antioxidant defenses in NH4+-supplied rice roots.HighlightNOS-mediated early NO burst plays an important role in alleviating oxidative damage induced by water stress, by enhancing the antioxidant defenses in roots supplemented with NH4+


2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Pradyumna Kumar Singh ◽  
Yuvraj Indoliya ◽  
Abhisekh Singh Chauhan ◽  
Surendra Pratap Singh ◽  
Amit Pal Singh ◽  
...  

2013 ◽  
Vol 305 (5) ◽  
pp. H620-H633 ◽  
Author(s):  
Virginie Bolduc ◽  
Nathalie Thorin-Trescases ◽  
Eric Thorin

Cognitive performances are tightly associated with the maximal aerobic exercise capacity, both of which decline with age. The benefits on mental health of regular exercise, which slows the age-dependent decline in maximal aerobic exercise capacity, have been established for centuries. In addition, the maintenance of an optimal cerebrovascular endothelial function through regular exercise, part of a healthy lifestyle, emerges as one of the key and primary elements of successful brain aging. Physical exercise requires the activation of specific brain areas that trigger a local increase in cerebral blood flow to match neuronal metabolic needs. In this review, we propose three ways by which exercise could maintain the cerebrovascular endothelial function, a premise to a healthy cerebrovascular function and an optimal regulation of cerebral blood flow. First, exercise increases blood flow locally and increases shear stress temporarily, a known stimulus for endothelial cell maintenance of Akt-dependent expression of endothelial nitric oxide synthase, nitric oxide generation, and the expression of antioxidant defenses. Second, the rise in circulating catecholamines during exercise not only facilitates adequate blood and nutrient delivery by stimulating heart function and mobilizing energy supplies but also enhances endothelial repair mechanisms and angiogenesis. Third, in the long term, regular exercise sustains a low resting heart rate that reduces the mechanical stress imposed to the endothelium of cerebral arteries by the cardiac cycle. Any chronic variation from a healthy environment will perturb metabolism and thus hasten endothelial damage, favoring hypoperfusion and neuronal stress.


2021 ◽  
Vol 11 (10) ◽  
pp. 4666
Author(s):  
Thanasekaran Jayakumar ◽  
Ming-Ping Wu ◽  
Joen-Rong Sheu ◽  
Chih-Wei Hsia ◽  
Periyakali Saravana Bhavan ◽  
...  

Pterostilbene (PTE), a natural stilbenoid occurring in grapes and berries, is recognized as a dimethylated analogue of resveratrol. This compound shows numerous notable pharmacological activities, including antiaging, anticancer, antidiabetes, antioxidant, and neuroprotection. This study investigates the anti-inflammatory properties of PTE in macrophage cells (RAW 264.7) against the lipoteichoic acid (LTA) stimulation. The expression of inflammatory tumor necrosis factor (TNF-α), interleukin-1β (IL-1 β), and inducible nitric oxide synthase (iNOS) and the content of nitric oxide (NO) were detected in LTA-induced cells. In addition, a Western blot assay was used to detect mitogen-activated protein kinases: extracellular signal-regulated kinase (ERK)1/2, p38 MAPK, and c-Jun N-terminal kinase (JNK). The phosphorylation of IκB and p65 and translocation of nuclear factor kappa B (NF-κB) were assessed by Western blot and immuno-fluorescence staining. The results showed that PTE significantly attenuated NO production and TNF-α, IL-1 β, and iNOS expression in LTA stimulated cells. Among the activation of ERK, JNK, and p38 in cells treated with LTA, PTE at higher concentration had only inhibited ERK activation. However, PTE blocked IκB phosphorylation, phosphorylation and nuclear translocation of p65NF-κB. Fascinatingly, PTE enhanced antioxidant defense molecules as verified by the enhanced heme oxygenase-1 (HO-1) expression, catalase (CAT) antioxidant enzyme, and non-enzymatic antioxidant, and reduced glutathione (GSH) in LTA-induced RAW 264.7 cells. These results suggest that PTE exerts an anti-inflammatory property via attenuating NF-κB/ERK signaling pathways as well as enriching antioxidant defense mechanisms.


2021 ◽  
Vol 9 (9) ◽  
pp. 1971
Author(s):  
Ki-Tae Kim ◽  
Jin-Woo Kim ◽  
Sun-Il Kim ◽  
Seonyoung Kim ◽  
Trung Hau Nguyen ◽  
...  

Oxidative stress is a phenomenon caused by an imbalance between the production of reactive oxygen species and antioxidant defenses. It plays an important role in numerous disease states, including chronic kidney disease, neurological disorders, cardiovascular diseases, diabetes, and cancer. Lactic acid bacteria (LAB) are known to have prominent antioxidant properties. Therefore, this study aimed to measure the antioxidant activity and anti-inflammatory potential of LAB isolated from animals for the efficient use of probiotics with host specificity. Antioxidant activity measurements of sixteen strains revealed that ABTS radical scavenging activities ranged from 26.3 to 57.4%, and DPPH free radical scavenging activities ranged from 4.7 to 13.5%. Based on the antioxidant activity assessment, five strains (Enterococcus faecium MG9003(YH9003), Enterococcus faecium MG9007(YH9007), Lactobacillus reuteri MG9012(YH9012), Lactobacillus fermentum MG9014(YH9014), and Pediococcus pentosaceus MG9015(YH9015)) were selected with the consideration of fermentation productivity (>1 × 109 CFU/g). The selected strains exhibited nitric oxide inhibition and inhibited inducible nitric oxide synthase and cyclooxygenase expression. Furthermore, probiotic properties, including intestinal adhesion and stability, were identified. Our results show that the selected animal-derived strains can be effective probiotic candidates for potential effects on animal hosts.


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