| Literature DB >> 15284058 |
Nader G Abraham1, Rita Rezzani, Luigi Rodella, Adam Kruger, Derek Taller, Giovanni Li Volti, Alvin I Goodman, Attallah Kappas.
Abstract
Heme oxygenase (HO)-1 represents a key defense mechanism against oxidative injury. Hyperglycemia produces oxidative stress and various perturbations of cell physiology. The effect of streptozotocin (STZ)-induced diabetes on aortic HO activity, heme content, the number of circulating endothelial cells, and urinary 8-epi-isoprostane PGF2alpha (8-Epi) levels in control rats and rats overexpressing or underexpressing HO-1 was measured. HO activity was decreased in hyperglycemic rats. Hyperglycemia increased urinary 8-Epi, and this increase was augmented in rats underexpressing HO-1 and diminished in rats overexpressing HO-1. The number of detached endothelial cells and O2- formation increased in diabetic rats and in hyperglycemic animals underexpressing HO-1 and decreased in diabetic animals overexpressing HO-1 compared with controls. These data demonstrate that HO-1 gene transfer in hyperglycemic rats brings about a reduction in O2- production and a decrease in endothelial cell sloughing. Upregulation of HO-1 decreases oxidant production and endothelial cell damage and shedding and may attenuate vascular complications in diabetes.Entities:
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Year: 2004 PMID: 15284058 DOI: 10.1152/ajpheart.01187.2003
Source DB: PubMed Journal: Am J Physiol Heart Circ Physiol ISSN: 0363-6135 Impact factor: 4.733