Assessment of DNA nucleo base oxidation and antioxidant defense in postmenopausal women under hormone replacement therapy.
OBJECTIVE
The aim of the present study was to evaluate oxidative stress by investing oxidatively damaged DNA AS Formamidopyrimidine DNA glycosylase (Fpg) -sensitive sites, glutathione peroxidase (GPx), superoxide dismutase (SOD) activities reduced glutathione (GSH) level and nitrite level as satble end product of in women receiving hormone replacement therapy (HRT).


METHODS
127 healthy postmenopausal women receiving HRT and 25 healthy control postmenopausal women were included in this study. Women receiving HRT, comprised surgical menopausal women who underwent surgery for benign conditions and received conjugated equine estrogen, 0.625 mg/day for 1 year (group 1), 5 years (group 2) and more than 10 years (group 3), spontaneous postmenopausal women received conjugated equine estrogen, 0.625 (Premarin) mg/day and medroxyprogesterone acetate, 2.5 mg/day (Premelle) for 1 year (group 4), 5 years (group 5) and more than 5 years (group 6).We investigated in the present study the effects of HRT on nitrite level and GSH level, activities of SOD and GPx and oxidative damage to DNA by comet assays by measuring levels of Fpg-sensitive sites.


RESULTS
Although no significant differences were found in the SOD activities, in total group receiving HRT, increased DNA oxidation (P<0.001) together with an increased GPx activity (P<0.001) and nitrite level (P<0.001) as well as a decreased GSH level (P < 0.05) as compared with controls were observed.


CONCLUSIONS
Estrogen alone or oestrogen in combination with progesterone and duration of use did not significantly alter the results. We evaluated that caused oxidative stress by investigating oxidative DNA damage as Fp-sensitive sites and GSH.NO levels in women receiving HRT.
Department of Biochemistry, Cerrahpasa Medical Faculty, University of Istanbul, Istanbul, Turkey. tulakcay@yahoo.com
Tülay
T
Akcay
Yildiz
Y
Dincer
E Ilker
EI
Saygili
Hakan
H
Seyisoğlu
Erdogan
E
Ertunğalp
D000704:Analysis of Variance; D000975:Antioxidants / Q000378:metabolism; D016022:Case-Control Studies; D004249:DNA Damage / Q000187:drug effects*; D043382:DNA-Formamidopyrimidine Glycosylase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D015914:Estrogen Replacement Therapy / Q000009:adverse effects / Q000379:methods; D004966:Estrogens, Conjugated (USP) / Q000008:administration & dosage / Q000009:adverse effects; D005260:Female; D005500:Follow-Up Studies; D020249:Hormone Replacement Therapy / Q000009:adverse effects / Q000379:methods*; D006801:Humans; D017258:Medroxyprogesterone Acetate / Q000008:administration & dosage / Q000009:adverse effects; D008875:Middle Aged; D010084:Oxidation-Reduction / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects*; D017698:Postmenopause / Q000097:blood / Q000187:drug effects*; D012016:Reference Values; D016896:Treatment Outcome
D000975:Antioxidants; D004966:Estrogens, Conjugated (USP); D017258:Medroxyprogesterone Acetate; D043382:DNA-Formamidopyrimidine Glycosylase