Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antioxidant activities of 17-beta-estradiol (E2) and other steroid hormones were studied by determining their effect on copper-catalyzed (cell-free) and mononuclear cell-mediated oxidation of low-density lipoproteins (LDL), as measured by the production of thiobarbituric acid-reactive substances (TBARS). The oxidation of LDL increased linearly with copper concentrations ranging from 0 to 10 mumol/L. E2 at a concentration of 1 mumol/L inhibited LDL oxidation by 37% to 62% at the various concentrations of copper. In a time-course study, E2 at 1 mumol/L delayed the onset of LDL oxidation in the presence of 5 mumol/L copper. E2 (1 mumol/L) inhibited TBARS production catalyzed by 5 mumol/L copper by 54%, compared with 60% inhibition by 1 mumol/L butylated hydroxytoluene (BHT), a known inhibitor of lipid peroxidation. Estriol at 5 mumol/L decreased LDL oxidation by 49%. Dehydroepiandrosterone (DHEA), testosterone, and estrone had no significant effects. E2 was also an effective inhibitor of mononuclear cell (MNC)-mediated oxidation of LDL, but had no effect on superoxide production by these cells. The onset of TBARS formation from cell-mediated LDL oxidation was also delayed by incubation with 1 mumol/L E2. The results indicate that estrogen may protect against atherosclerosis by inhibiting lipoprotein oxidation.
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PMID:The inhibition of low-density lipoprotein oxidation by 17-beta estradiol. 132 22

Estriol (E3) has little effect on the female genitals. E3 is used in hormone replacement therapy, particularly in Europe and Japan, since it obviates the need for progestin administration. However, the effect of E3 on atherosclerosis has not been elucidated. In this study, we evaluated the effect of E3 on the progression of atherosclerosis in a rabbit model. Thirty-six rabbits total were used. Twenty-eight were bilaterally oophorectomized, and 8 were not. The rabbits were divided into 5 groups and treated for 12 weeks as follows. Gp I (n = 8) was fed a high cholesterol diet (HCD; standard diet plus 0.5% cholesterol); Gp II (n = 8) was fed a HCD with E3 (0.3 mg/kg/day); Gp III (n = 8) was fed a HCD with 17beta estradiol (E2) (0.1 mg/kg/day); Gp IV (n = 8), the non oophorectomized group, was fed a HCD; and Gp NC was oophorectomized (n = 4), and fed a regular diet. E3 treatment increased the plasma E2 and E3 levels in Gp II. The plasma lipid levels were not altered by the E2 or E3 treatment. A HCD diminished the acetylcholine-induced NO mediated relaxation in the thoracic aorta. The E2 treatment (Gp III) and E3 treatment (Gp II) restored the aortic basal NO release and the aortic cyclic GMP levels, particularly effectively in the E3 group. E3 treatment also decreased the atherosclerotic area, and its effect was comparable with E2 (surface involvement: 41.2 +/- 5.1% in Gp I; 10.1 +/- 2.7% in Gp II; and 6.5 +/- 1.3% in Gp III). All four hyperlipidemic groups showed an increase of eNOS mRNA in the aortae, and this was especially pronounced in Gps II and III. The level of peroxynitrite, as determined by immunohistochemical nitrotyrosine staining, was lower in Gps II and III than in Gp I. E3 strongly activates NO-mediated systems, and could play a role in retarding the progression of atherosclerosis and in stabilizing atheroma.
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PMID:Estriol retards and stabilizes atherosclerosis through an NO-mediated system. 1202 Jul 46

Oxidative stress is characterized by an overweight of pro-oxidants against antioxidant forces and is associated with atherosclerosis, aging, and reproductive complications. Placenta is the major source of pro-oxidant agents, antioxidant enzyme-systems, and hormones and is able to keep the lipid peroxidation under control in normal pregnancy. As oxidation processes are increased in pregnancy, we would expect a shortening of lag phase of low density lipoprotein (LDL)-oxidation. LDL oxidation assessed by measuring conjugated diene formation is a marker for the early part of lipid peroxidation process and the balance of pro-oxidants and antioxidants influences length of lag phase. Our results show that resistance of LDL oxidation is unchanged during normal pregnancy in the second and third trimester. Only antioxidants are able to protect LDL. Estriol is an antioxidant, increases the lag-phase of LDL-oxidation in vitro, and its serum concentration raises enormous during late pregnancy. Thus the biological role of high levels of estriol during pregnancy may be part of the self-protection to limit oxidative damages.
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PMID:Placental defence is considered sufficient to control lipid peroxidation in pregnancy. 1561 65