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Estrogen may lower women's risk of heart disease by working as damper on inflammation

were drawn at two, four, six and 24 hours after the injection.

Researchers measured the generation of reactive oxygen species, or oxygen free radicals -- components known to damage cells in blood-vessel walls and induce inflammation -- in specific cells (mononuclear cells), molecules (polymorphonuclear leukocytes) and in plasma.

They also assessed concentrations of three factors known to be markers of the inflammatory process: intranuclear nuclear factor-(B (NF-(B), C-reactive protein (CRP) and plasminogen activator inhibitor-1 (PAI-1).

Results showed that estrogen significantly inhibited the generation of free radicals by mononuclear cells and leukocytes, with peak inhibition -- 39.9 percent and 47.3 percent respectively -- reached at four hours after estrogen infusion.

NF-(B activity fell to a low of 24 percent at six hours after infusion, and C-reactive protein concentration dropped a maximum of 19.5 percent at four hours, results showed. In addition, plasminogen activator inhibitor-1 fell nearly 50 percent at six hours.

'These early results allow us to understand the mechanism and to say that estrogen works in this fashion," said Dandona, who plans to conduct a similar study in postmenopausal women.

"It should be possible to separate estrogen's feminizing effects from its anti-inflammatory effects," he said. "In the long run, estrogen may prove helpful as an addition to current therapy in the treatment and prevention of heart disease."


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Contact: Lois Baker
ljbaker@buffalo.edu
716-645-5000 x1417
University at Buffalo
20-Jun-2002


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