Estrogen’s role as an inhibitor of toxic-free radicals incerebral blood vessels may be a key reason why premenopausal women havea lower stroke risk than men.
According to UC Irvine School ofMedicine researchers, estrogen has a powerful and positive influence onwomen’s health by increasing the energy production efficiency ofmitochondria – the tiny power plants that provide cells the energy theyneed to function. And in doing so, the hormone inhibits themitochondrial production of free radical oxygen molecules. Previousstudies have shown that excessive amounts of these radical elements inthe body, through a process called oxidative stress, can damage bloodvessels and lead to stroke or degenerative disease.
In the UCIstudy, Dr. Vincent Procaccio of the Center for Molecular andMitochondrial Medicine and Genetics and colleagues discovered estrogenreceptors in vascular mitochondrial cells. To see how mitochondriafunctioned with deficient estrogen levels, they removed the ovariesfrom test rats, which suppressed any hormone influence, and identifieda significant increase in radical oxygen molecule levels and a declinein the capacity for mitochondria to produce energy. In rats treatedwith doses of estrogen, however, vascular mitochondria produced energymore efficiently with lower amounts of damaging free radicals.
“Wewant to find out more how estrogen can protect blood vessels in thebrain,” said Procaccio, also an assistant professor of pediatrics. “Andwhen we gain a fuller understanding, we hopefully can figure out howbest to realize potential benefits of hormone replacement therapies.Also, learning the mechanisms by which estrogen is beneficial to braincirculation may give us new ideas about how to protect against stroke.”
Spurredby recent findings of the Women’s Health Initiative, there is growingdebate over the effects of estrogen and the risk of cardiovasculardisease and stroke. While women aged 30 to 50 have about five timesless risk of stroke than men, this difference disappears when womenreach menopause. Research studies show that estrogen protects animalsfrom experimental stroke, but recent clinical trials with certainhormone replacement therapies in older women did not show protectionfrom stroke.
Study results appear on the online version ofMolecular Pharmacology. Chris Stirone, Sue P. Duckles and Diana N.Krause of the UCI Department of Pharmacology assisted with the study.The National Institutes of Health provided support.
Mitochondriaare the power plants of cells responsible for burning the calories inour diet with the oxygen that we breathe to generate carbon dioxide,water and the energy for our cells. The cellular energy is used for twopurposes, to generate heat to maintain our body temperature and tosynthesize ATP (adenosine triphosphate), a chemical form of energywhich permits us to do work such as exercise, think, write, and makeand repair cells and tissues.
When the mitochondria burn ourdietary fuel, they also generate a toxic by-product called oxygenradicals, the mitochondrial equivalent to the smoke generated bycoal-burning power plants. Oxygen radicals, in turn, damage themitochondria and the surrounding cell. When sufficient oxidative damageaccumulates in the mitochondria and the cell, the cell dies. Hence, thechronic level of mitochondrial oxidative stress is believed to helpdetermine an individuals aging rate and susceptibility to a variety ofdiseases such as cardiovascular disease, stroke, diabetes, memory loss,forms of deafness and vision loss.
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