Myoglobin Protects the Heart from Inducible Nitric-oxide Synthase (iNOS)-mediated Nitrosative Stress

Mammalian target of rapamycin (mTOR) has been recognized with potential immunomodulatory properties playing an important role in various physiopathological processes including ischemia–reperfusion (I/R) injury. I/R injury stimulate reactive oxygen and nitrogen species by activating nicotinamide adenine dinucleotide phosphate oxidase and inducible nitric oxide synthase, respectively. Controversial results have been obtained in different I/R models following localized I/R; however, the precise role of the mTOR signaling pathway remains undefined. The objective of the current study was to evaluate the role of the mTOR in oxidative–nitrosative stress and inflammation in hindlimb I/R-induced injury in target and remote organ injuries. In rats subjected to I/R, an increased expression of ribosomal protein S6 (rpS6), inhibitor κB (IκB)-α, nuclear factor-κB (NF-κB) p65, inducible nitric oxide synthase, cyclooxygenase 2, gp91phox, and levels of tumor necrosis factor α, nitrite, nitrotyrosine, malondialdehyde and the activities of myeloperoxidase and catalase in the tissues and (or) sera were detected. Treatment with rapamycin, a selective inhibitor of mTOR, reversed all the I/R-induced changes as manifested by its anti-inflammatory and antioxidant effects in kidney and gastrocnemius muscle of rats. Collectively, these findings suggest that rapamycin protects against I/R-induced oxidative–nitrosative stress and inflammation leading to organ injuries via suppression of mTOR/IκB-α/NF-κB signaling pathway.

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Cytoglobin regulates cell respiration and nitrosative stress through NO dioxygenation and co‐localizes with inducible nitric oxide synthase during vascular injury.

The FASEB Journal ◽

10.1096/fasebj.23.1_supplement.852.3 ◽

2009 ◽

Vol 23 (S1) ◽

Author(s):

Katharine E. Halligan ◽

Frances Jourd'heuil ◽

David Jourd'heuil

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Inducible Nitric Oxide Synthase ◽

Vascular Injury ◽

Nitrosative Stress ◽

Cell Respiration ◽

Oxide Synthase ◽

Inducible Nitric Oxide

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A comparative clinical study on the generation of nitrosative stress in cataractous lenses of smokers and non-smoker tobacco patients

European Journal of Ophthalmology ◽

10.1177/1120672118785101 ◽

2018 ◽

Vol 29 (2) ◽

pp. 178-182 ◽

Cited By ~ 1

Author(s):

Thirugnanasambandhar Sivasubramanian Anitha ◽

Krishnagopal Srikanth ◽

Subrayan Suganya ◽

Subramanian Muthukumar

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Inducible Nitric Oxide Synthase ◽

Nitrosative Stress ◽

Enzyme Linked Immunosorbent Assay ◽

Department Of Ophthalmology ◽

Gandhi Medical College ◽

Oxide Synthase ◽

Inducible Nitric Oxide ◽

Tobacco Chewing

Aim: To quantify the levels of nitric oxide, inducible nitric oxide synthase, and 3-nitrotyrosine in cataractous lenses of smokers and smokers who chewed tobacco in comparison with non-smokers and non-smokers who chewed tobacco. Study design: A total of 80 cataractous lenses from smokers, non-smokers, smokers with tobacco chewing habit, and non-smokers with tobacco chewing habit were collected from the patients who had enrolled in the Department of Ophthalmology, Mahatma Gandhi Medical College & Research Institute, Puducherry. Methods: Levels of nitric oxide, inducible nitric oxide synthase, and 3-nitrotyrosine were quantified using commercially available enzyme-linked immunosorbent assay kits. Results: The mean concentrations of lens nitric oxide, inducible nitric oxide synthase, and 3-nitrotyrosine are as follows: (a) smokers—112.01, 59.57, and 88.91 µmol/L; (b) smokers who chewed tobacco—175.15, 93.95, and 128.72 µmol/L; (c) non-smokers—76.15, 40.65, and 70.20 µmol/L; and (d) non-smokers who chewed tobacco—96.56, 52.87, and 83.88 µmol/L, respectively. Conclusion: Nitric oxide, inducible nitric oxide synthase, and 3-nitrotyrosine at high levels are the major causative agents for cataractogenesis. The results of this study suggest that smoking and tobacco chewing habit generate nitrosative stress that could enhance the pathogenesis for early cataractogenesis.

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