Nitric oxide as a cellular antioxidant: A little goes a long way

Hummel, Stephen G.; Fischer, Anthony J.; Martin, Sebastian; Schäfer, Freya; Buettner, Garry R.

doi:10.1016/j.freeradbiomed.2005.08.047

Cited by 124 publications

(60 citation statements)

References 41 publications

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“…Specifically, cigarette smoke activates patho- Increased by CS (7,57) Reference numbers are shown in parentheses. eNO, exhaled nitric oxide; GSH, reduced glutathione; ROS, reactive oxygen species; TEAC, trolox equivalent antioxidant capacity.…”

Section: Cs Oxidative Stress and Immune Response In Copdmentioning

confidence: 99%

Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

Zuo

Sergakis

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

210

139

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Cigarette smoking (CS) can impact the immune system and induce pulmonary disorders such as chronic obstructive pulmonary disease (COPD), which is currently the fourth leading cause of chronic morbidity and mortality worldwide. Accordingly, the most significant risk factor associated with COPD is exposure to cigarette smoke. The purpose of the present study is to provide an updated overview of the literature regarding the effect of CS on the immune system and lungs, the mechanism of CS-induced COPD and oxidative stress, as well as the available and potential treatment options for CS-induced COPD. An extensive literature search was conducted on the PubMed/Medline databases to review current COPD treatment research, available in the English language, dating from 1976 to 2014. Studies have investigated the mechanism by which CS elicits detrimental effects on the immune system and pulmonary function through the use of human and animal subjects. A strong relationship among continued tobacco use, oxidative stress, and exacerbation of COPD symptoms is frequently observed in COPD subjects. In addition, therapeutic approaches emphasizing smoking cessation have been developed, incorporating counseling and nicotine replacement therapy. However, the inability to reverse COPD progression establishes the need for improved preventative and therapeutic strategies, such as a combination of intensive smoking cessation treatment and pharmaceutical therapy, focusing on immune homeostasis and redox balance. CS initiates a complex interplay between oxidative stress and the immune response in COPD. Therefore, multiple approaches such as smoking cessation, counseling, and pharmaceutical therapies targeting inflammation and oxidative stress are recommended for COPD treatment.

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Section: Cs Oxidative Stress and Immune Response In Copdmentioning

confidence: 99%

Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

Zuo

Sergakis

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

210

139

View full text Add to dashboard Cite

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“…For instance, nitric oxide synthesis inhibitors by limiting •NO production can limit PN formation. However, they also have the potential to interfere with the physiological roles for which •NO is responsible, including antioxidant effects, due to its important role as a scavenger of lipid peroxyl radicals (e.g., LOO•+•NO →LOONO) [61]. Another approach to blocking post-traumatic radical formation is the inhibition of the arachidonic acid cascade, during which the formation of O 2…”

Section: Overview Of Antioxidant Mechanistic Approachesmentioning

confidence: 99%

Antioxidant Therapies for Acute Spinal Cord Injury

2011

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Summary:One of the most investigated molecular mechanisms involved in the secondary pathophysiology of acute spinal cord injury (SCI) is free radical-induced, iron-catalyzed lipid peroxidation (LP) and protein oxidative/nitrative damage to spinal neurons, glia, and microvascular cells. The reactive nitrogen species peroxynitrite and its highly reactive free radicals are key initiators of LP and protein nitration in the injured spinal cord, the biochemistry, and pathophysiology of which are first of all reviewed in this article. This is followed by a presentation of the antioxidant mechanistic approaches and pharmacological compounds that have been shown to have neuroprotective properties in preclinical SCI models. Two of these, which act by inhibition of LP, are high-dose treatment with the glucocorticoid steroid methylprednisolone (MP) and the nonglucocorticoid 21-aminosteroid tirilazad, have been demonstrated in the multicenter NASCIS clinical trials to produce at least a modest improvement in neurological recovery when administered within the first 8 hours after SCI. Although these results have provided considerable validation of oxidative damage as a clinically practical neuroprotective target, there is a need for the discovery of safer and more effective antioxidant compounds for acute SCI.

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“…By this route, reactive nitrogen and oxygen species may act in concert to inactivate the key metabolic enzymes and cause lipid peroxidation and DNA strand breaks that result in irreversible cell injury and death (Radi, 2004;(Hummel et al, 2006).…”

Section: Molecular Nitric Oxide Targets In Cellsmentioning

confidence: 99%