Antioxidant therapies / vascular complications of diabetes

ironjustice@aol.com · medicine forum Guru Joined: 28 Apr 2005 Posts: 1522

J Biol Chem. 2005 Apr 25; [Epub ahead of print] Related Articles, Links

Reactive carbonyls and polyunsaturated fatty acids produce a hydroxyl
radical-like species: A potential pathway for oxidative damage of
retinal proteins in diabetes.

Pennathur S, Ido Y, Heller JI, Byun J, Danda R, Pergola P, Williamson
JR, Heinecke JW.

Department of Medicine, Division of Endocrinology, Diabetes and
Metabolism, University of Washington, Seattle, WA 98195.

The pattern of oxidized amino acids in aortic proteins of nonhuman
primates suggests that a species resembling hydroxyl radical damages
proteins when blood glucose levels are high. However, recent studies
argue strongly against a generalized increase in diabetic oxidative
stress, which might instead be confined to the vascular wall. Here, we
describe a pathway for glucose-stimulated protein oxidation and provide
evidence of its complicity in diabetic microvascular disease. Low
density lipoprotein incubated with pathophysiological concentrations of
glucose became selectively enriched in ortho-tyrosine and
meta-tyrosine, implicating a hydroxyl radical-like species in protein
damage. Model system studies demonstrated that the reaction pathway
requires both a reactive carbonyl group and a polyunsaturated fatty
acid, involves lipid peroxidation, and is blocked by the carbonyl
scavenger aminoguanidine. To explore the physiological relevance of the
pathway, we used mass spectrometry and HPLC to quantify oxidation
products in control and hyperglycemic rats. Hyperglycemia raised levels
of ortho-tyrosine, meta-tyrosine, and oxygenated lipids in the retina,
a tissue rich in polyunsaturated fatty acids. Rats that received
aminoguanidine also did not show this increase in protein and lipid
oxidation. In contrast, hyperlipidemia in the absence of hyperglycemia
failed to increase protein and lipid oxidation products in the retina.
Our observations suggest that generation of a hydroxyl radical-like
species by a carbonyl/polyunsaturated fatty acid pathway might promote
localized oxidative stress in tissues vulnerable to diabetic damage.
This raises the possibility that antioxidant therapies that
specifically inhibit the pathway might delay the vascular complications
of diabetes.

PMID: 15855169 [PubMed - as supplied by publisher]

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Sarah · medicine forum beginner Joined: 30 Apr 2005 Posts: 1

At first glance I would label this post as a precursor spamming ad.
Aminoguanidine is sold as a supplement and is touted on many anti-ageing web
sites. The fact that it was multi-posted to 5 newsgroups furthers this
belief.

Sarah
Type 1

<ironjustice@aol.com> wrote in message
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John Que · medicine forum Guru Wannabe Joined: 30 Apr 2005 Posts: 154

Ironjustice is a lunatic in my personal opinion
as he seems to think all ills springs from iron or its
cations. What ever your opinion comes to be of aminoguanidine
don't let ironboy affect it.

"Sarah" <sarahpa1980nospam@yahoo.com> wrote in message
news:25mdnW1ZlM01QO7fRVn-rQ@giganews.com...

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