Health Evaluation and Promotion
Online ISSN : 1884-4103
Print ISSN : 1347-0086
ISSN-L : 1347-0086
40th JHEP conference 2012
Basic and clinical study of free radicals (active molecule species)
— Analysis from thermal injury —
Hajime Inoue
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JOURNAL FREE ACCESS

2012 Volume 39 Issue 5 Pages 589-595

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Abstract
 It is well known for superoxide anion, hydroxyl peroxide, nitric oxide and peroxynitrite to be the free radicals. To protect the living body from the oxidative stress with the free radicals production, we have the various reduction functions. It is called the Redox control. The NO was discovered as a gaseous mediator for the dilation of vascular smooth muscle produced by vascular endothelial cells. As the nitric oxide was discovered from vascular endothelial cells at first, it was thought that the mediator was only concerned to regulate the circulation. However, the NO does not only function as neurotransmitter either, and it is known that NO produced with inflammatory reaction is associated with biophylaxis. On the other hand, the produced NO is converted into extremely potent reactive ONOO- in presence of O2- produced at the same time in site of inflammation non-enzymatically and these induce nitration with the oxidation of the surrounding tissue and cause tissue injury. The large amounts of inflammatory mediators are released from the surrounding region of thermal injury by thermal stimulation, and then the various kinds of reactive molecular species are also produced in the same region. These inflammatory factors and free radicals cause a systemic inflammatory response syndrome (SIRS) by affecting to normal tissues and organs. The author reported that the inhibition of NO production at acute inflammatory phase (0.5~3.0 hours after thermal injury) caused by invasive stimulation of heat induced the potent anti-inflammatory effect. Especially, NO did not affect the inflammatory reaction, but ONOO- which reacted non-enzymatically under the presence of O2- induced tissue damage by nitrating a surrounding tissue. In other words, it means that the nonenzymatic responses between active molecular species are fraught with the risk of the tissue damage as far as we breathe. The redox control failure may affect acceleration of aging and the induction of the disease.
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© 2012 Japan Society of Health Evaluation and Promotion
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