Postmenopausal hormone replacement therapy use decreases oxidative protein damage

• Published in: Gynecologic and obstetric investigation Vol. 54; no. 2; p. 88
• Main Authors: Telci, Ayşegül, Cakatay, Ufuk, Akhan, Süleyman E, Bilgin, Murat E, Turfanda, Abdullah, Sivas, Ahmet
• Format: Journal Article
• Language: English
• Published: Switzerland 01-01-2002
• Subjects: Blood Proteins - metabolism; Case-Control Studies; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Estrogen Replacement Therapy; Estrogens, Conjugated (USP) - administration & dosage; Female; Glutathione - blood; Humans; Medroxyprogesterone Acetate - administration & dosage; Middle Aged; Nitric Oxide - blood; Oxidative Stress; Postmenopause; Sulfhydryl Compounds - blood; Triglycerides; Tyrosine - analogs & derivatives; Tyrosine - blood
• DOI: 10.1159/000067718
• ISSN: 0378-7346

The aim of this study is to evaluate oxidative protein damage (OPD) by investigating protein carbonyl (PCO) and nitrotyrosine (NT) levels, oxidative stress by total thiol (T-SH), erythrocyte glutathione (GSH) and nitric oxide (NO) levels in women receiving hormone replacement therapy (HRT).
To examine the influence of oxidative stress on OPD, we studied 12 postmenopausal women who had received HRT for 6 months, and 13 postmenopausal women who did not receive HRT, as the control group. All subjects were non-smokers. Blood samples were drawn in the fasting state and processed within 1 h of collection. For NT and NO, serum samples were stored at -70 degrees C until analysis; all other parameters were determined on the same day of collection.
After 6 months, plasma PCO and T-SH levels were decreased, GSH and NO levels were increased, and NT levels were not changed in 12 postmenopausal women receiving HRT. Except the NT levels, the rest of the parameters did not significantly change in the control group. Interestingly, mean NT levels in the control group increased significantly.
A crucial part of the protective effect of HRT on the cardiovascular system arises secondary to the interaction between estrogen and vessel wall. Our results suggest that an important component of the mechanism underlying this interaction may depend on estrogen's antioxidant effect and its preventive role in OPD.