Abstract
As women undergo menopause, circulating concentrations of estrogen decrease. The relative
estrogen deprivation in postmenopausal women is associated with physiological changes
and increased risk of several diseases, including cardiovascular disease. Studies
in animals have shown that exogenous estrogen inhibits atherosclerosis, the underlying
cause cardiovascular disease. Ongoing clinical trials will soon data for the effect
of exogenous estrogen on cardiovascular disease in postmenopausal women. Estrogen
has a number of effects that could influence atherogenesis and cardiovascular disease.
Estrogens have favorable effects on lipoproteins, but such effects can only account
for part of the protection from cardiovascular disease that appears to be conferred
by estrogen. Evidence suggests that estrogens can have both prooxidant and antioxidant
effects. However, the available evidence suggests that in vivo physiological concentrations
of estrogen may have a modest antioxidant activity, and prooxidant activity is unlikely.
The antioxidant activity of estrogens and inhibition by estrogens of cellular processes
that are thought to promote atherosclerosis are likely be additional mechanism(s)
by which estrogen inhibits atherosclerosis and cardiovascular disease, but more work
is needed. Studies of some effects of estrogens on atherogenic processes in isolated
cells need to be extended to the whole animal. The influence of estrogen receptors
on inhibition atherosclerosis by estrogen needs to be clarified. Future studies should
be designed to investigate separately the estrogenic and antioxidant activities of
estrogens and estrogen analogs. Investigations of the antioxidant activities of estrogens
should include careful consideration of the interaction of estrogens with endogenous
antioxidants and fatty acid saturation, and more attention should be paid to the potential
for estrogens to inhibit intraarterial oxidation.
Keywords:
Estrogen - atherosclerosis - antioxidants - lipid peroxidation - free radical - nitric
oxide - LDL receptor - nitric oxide synthase
