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Cerebral vascular dysfunction mediated by superoxide in hyperhomocysteinemic mice
Sanjana Dayal1, Erland Arning, Teodoro Bottiglieri
1Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA.
Stroke
|June 5, 2004
Summary
High methionine diets induce hyperhomocysteinemia in mice, impairing cerebral arteriole function. Superoxide production mediates this endothelial dysfunction, highlighting its role in stroke risk.
Area of Science:
- Cardiovascular Research
- Neuroscience
- Vascular Biology
Background:
- Hyperhomocysteinemia is an emerging stroke risk factor.
- Its impact on cerebral vascular function remains unclear.
- This study investigates hyperhomocysteinemia's effects on cerebral arterioles.
Purpose of the Study:
- To test if chronic hyperhomocysteinemia causes endothelial dysfunction in mouse cerebral arterioles.
- To determine if superoxide mediates this dysfunction.
Main Methods:
- Mice (Cbs+/- and wild type) were fed control or high-methionine diets for 10-12 months.
- Cerebral arteriole dilation was measured in vivo.
- Vascular superoxide levels were assessed using dihydroethidium (DHE) staining.
Main Results:
- High-methionine diet elevated plasma homocysteine in both mouse groups.
- Endothelium-dependent vasodilation to acetylcholine was impaired by the diet.
- Superoxide scavenger tiron restored vasodilation, and superoxide levels were elevated.
- Endothelium-independent vasodilation to nitroprusside was unaffected.
Conclusions:
- Superoxide is a key mediator of endothelial dysfunction.
- Diet-induced hyperhomocysteinemia impairs cerebral arteriole function.
- This dysfunction is linked to increased superoxide production.