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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


VASCULAR REACTIVITY IN OXIDATIVE STRESS
Abstract number: PF16-131

Tkachenko1 M.N., Kotsjuruba1 A.V., Sagach1 V.F.

1A.A. Bogomolets Institute of Physiology NAS Ukraine, Kiev, Ukraine [email protected]

Aim: 

Nitric oxide (NO)-dependent mechanisms of vascular regulation and metabolism of the reactive oxygen species (ROS) and stable NO metabolites were studied in the aorta of BALB/c mice in conditions of oxidative stress induced by long-term exposure to low doses of external g-irradiation.

Methods: 

Endothelium-dependent and endothelium-independent vascular reactions of relaxation, content of ROS and stable NO metabolites were studied on aorta preparations of two groups of BALB/c mice: I – control (6-8 mo.); II – irradiated (equivalent dose of 96.9 mcSv/h) 8-mo. mice (cumulative dose of 0.43 Sv).

Results: 

Low doses of radiation were found to inhibit endothelium-dependent reactions of aortal smooth muscles to acetylcholine and to partially impair endothelium-independent relaxation to sodium nitroprusside. This is accompanied by a formation of high levels of superoxide anion, hydroxyl radical, and significant changes in the pools of stable NO metabolites (nitrite- and nitrate-anions). In increased simultaneous generation of .O2- and NO they may bind and thus form a toxic substance peroxynitrite. This can be confirmed by the low doses of nitrite, which are formed spontaneously in the presence of molecular oxygen against the background of increased or control levels of nitrate, which is formed mainly at the degradation of peroxynitrite, i.e. at high levels of superoxide anion.

Conclusion: 

Long-term exposure to low doses of g-irradiation results in the development of oxidative stress with an increase of ROS content and disturbance of vascular reactivity.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PF16-131

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