Nitric Oxide Prevents Fe Deficiency-Induced Photosynthetic Disturbance, and Oxidative Stress in Alfalfa by Regulating Fe Acquisition and Antioxidant Defense

Iron (Fe) deficiency impairs photosynthetic efficiency, plant growth and biomass yield. This study aimed to reveal the role of nitric oxide (NO) in restoring Fe-homeostasis and oxidative status in Fe-deficient alfalfa. In alfalfa, a shortage of Fe negatively affected the efficiency of root andshoot length, leaf greenness, maximum quantum yield PSII (Fv/Fm), Fe, S, and Zn accumulation, as well as an increase in H2O2 accumulation. In contrast, in the presence of sodium nitroprusside (SNP), a NO donor, these negative effects of Fe deficiency were largely reversed. In response to the SNP, the expression of Fe transporters (IRT1, NRAMP1) and S transporter (SULTR1;2) genes increased in alfalfa. Additionally, the detection of NO generation using fluorescence microscope revealed that SNP treatment increased the level of NO signal, indicating that NO may act as regulatory signal in response to SNP in plants. Interestingly, the increase of antioxidant genes and their related enzymes (Fe-SOD, APX) in response to SNP treatment suggests that Fe-SOD and APX are key contributors to reducing ROS (H2O2) accumulation and oxidative stress in alfalfa. Furthermore, the elevation of Ascorbate-glutathione (AsA-GSH) pathway-related genes (GR and MDAR) Fe-deficiency with SNP implies that the presence of NO relates to enhanced antioxidant defense against Fe-deficiency stress.

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

Hypertension Research ◽

10.1038/hr.2011.180 ◽

2011 ◽

Vol 35 (4) ◽

pp. 418-425 ◽

Cited By ~ 44

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

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Inducible nitric oxide synthase augments injury elicited by oxidative stress in rat cardiac myocytes

AJP Cell Physiology ◽

10.1152/ajpcell.1998.274.1.c245 ◽

1998 ◽

Vol 274 (1) ◽

pp. C245-C252 ◽

Cited By ~ 27

Author(s):

Junsuke Igarashi ◽

Masashi Nishida ◽

Shiro Hoshida ◽

Nobushige Yamashita ◽

Hiroaki Kosaka ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Cardiac Myocytes ◽

Myocardial Injury ◽

No Production ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

No Donor ◽

Oxide Synthase ◽

Gpx Activity

The effects of nitric oxide (NO) produced by cardiac inducible NO synthase (iNOS) on myocardial injury after oxidative stress were examined. Interleukin-1β induced cultured rat neonatal cardiac myocytes to express iNOS. After induction of iNOS,l-arginine enhanced NO production in a concentration-dependent manner. Glutathione peroxidase (GPX) activity in myocytes was attenuated by elevated iNOS activity and by an NO donor, S-nitroso- N-acetyl-penicillamine (SNAP). Although NO production by iNOS did not induce myocardial injury, NO augmented release of lactate dehydrogenase from myocyte cultures after addition of H2O2(0.1 mM, 1 h). Inhibition of iNOS with Nω-nitro-l-arginine methyl ester ameliorated the effects of NO-enhancing treatments on myocardial injury and GPX activity. SNAP augmented the myocardial injury induced by H2O2. Inhibition of GPX activity with antisense oligodeoxyribonucleotide for GPX mRNA increased myocardial injury by H2O2. Results suggest that the induction of cardiac iNOS promotes myocardial injury due to oxidative stress via inactivation of the intrinsic antioxidant enzyme, GPX.

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Mercury Exposure and Endothelial Dysfunction

International Journal of Toxicology ◽

10.1177/1091581815589766 ◽

2015 ◽

Vol 34 (4) ◽

pp. 300-307 ◽

Cited By ~ 13

Author(s):

Swati Omanwar ◽

M. Fahim

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Endothelial Dysfunction ◽

Vascular Endothelium ◽

Circulatory System ◽

Vital Role ◽

Mercury Exposure ◽

And Function ◽

The Impact ◽

And Oxidative Stress

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.

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