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Pathways of oxidative damage to skel...

Judge, Andrew.

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Pathways of oxidative damage to skeletal muscle after an acute bout of contractile claudication.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Pathways of oxidative damage to skeletal muscle after an acute bout of contractile claudication./
作者:	Judge, Andrew.
面頁冊數:	60 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0021.
Contained By:	Dissertation Abstracts International65-01B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3120122
ISBN:	0496674943

Pathways of oxidative damage to skeletal muscle after an acute bout of contractile claudication.
Judge, Andrew.

Pathways of oxidative damage to skeletal muscle after an acute bout of contractile claudication. - 60 p.

Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0021.

Thesis (Ph.D.)--University of Florida, 2003.

A limited number of studies have shown an increase in products of lipid peroxidation in the plasma of claudicants following exercise. Previously, we have used an animal model to mimic the condition of exercise claudication to show oxidative damage and edema within the muscle. Using this same model, we investigated the sources of this oxidative damage in the gastrocnemius muscle, focusing on xanthine oxidase and neutrophils, in addition to determining the role iron plays in the exercising claudicant.

ISBN: 0496674943Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Pathways of oxidative damage to skeletal muscle after an acute bout of contractile claudication.
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245 1 0 $a Pathways of oxidative damage to skeletal muscle after an acute bout of contractile claudication.
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500 $a Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0021.
500 $a Chair: Stephen Dodd.
502 $a Thesis (Ph.D.)--University of Florida, 2003.
520 $a A limited number of studies have shown an increase in products of lipid peroxidation in the plasma of claudicants following exercise. Previously, we have used an animal model to mimic the condition of exercise claudication to show oxidative damage and edema within the muscle. Using this same model, we investigated the sources of this oxidative damage in the gastrocnemius muscle, focusing on xanthine oxidase and neutrophils, in addition to determining the role iron plays in the exercising claudicant.
520 $a The increase in lipid hydroperoxides, seen in claudicant muscle, was attenuated with independent inhibition of xanthine oxidase activity, depletion of neutrophils, and chelation of iron. An additional marker of lipid peroxidation, 4 hydroxy-2-nonenal (HNE), was also attenuated by depletion of neutrophils. HNE is formed from oxidant-induced decomposition of lipid hydroperoxides, but actually binds to amino acid side chains of proteins, potentially affecting their function.
520 $a Protein oxidation, indicated by an increased level of protein carbonyls, was significantly increased in claudicant muscle, but attenuated by depletion of neutrophils.
520 $a Since oxidants have the potential to modify membrane macromolecules we also investigated LDH activity, as an indicator of muscle cell membrane permeability, and wet/dry ratio as a marker of edema---relective of vascular membrane permeability. LDH activity was decreased in claudicant muscles, reflecting loss of the cytosolic enzyme due to membrane alterations. This loss was attenuated with independent inhibition of xanthine oxidase activity, depletion of neutrophils and chelation if iron. Edema, however, was only attenuated by neutrophil depletion.
520 $a Our findings suggest that neutrophils are the predominant source of oxidants following exercise claudication, and the sole cause of edema. However, we also show that xanthine oxidase-derived oxidants contribute to lipid peroxidation and are chemotaxic to neutrophils. Finally, we show that chelation of iron also attenuates lipid peroxidation, despite an increase in xanthine oxidase and neutrophils, demonstrating irons role in propogating oxidant reactions.
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