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DHEA administration changes antioxidant enzymes in Wistar rat hearts
Author(s) -
jacob maria helena vianna metello,
janner daiane da rocha,
bellóklein adriane,
ribeiro maria flavia marques
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1153.2
Subject(s) - dehydroepiandrosterone , endocrinology , oxidative stress , medicine , lipid peroxidation , superoxide dismutase , antioxidant , chemistry , glutathione , hormone , catalase , enzyme , biochemistry , androgen
Dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) are the major circulating steroid hormones of adrenal cortex. Epidemiological studies show an inverse correlation between DHEA/DHEAS plasma concentration and mortality, with increased risks of cardiovascular disease. It is interesting to search how DHEA might act in myocardial oxidative stress, once this steroid has been largely used as a hormone of replacement therapy as well as a dietary supplement. DHEA was administrated to 3 month‐male Wistar rats (n=5 per group) in distinct doses: 1, 10 and 50 mg/kg i.p. After 6 or 24 hours, rats were killed and heart homogenates were pepared to quantify lipid peroxidation (LPO), activities and concentration of superoxide dismutase (SOD), catalase (CAT) and glutathione‐S‐transferase (GST), concentration of p‐ Akt/Akt ratio and 4‐hydroxy‐2‐nonenal (HNE). Data were evaluated by one‐way ANOVA followed by the SNK test. After 6 hours, LPO increased in groups 1 and 10 mg/kg when compared to control (69% and 98%, respectively). SOD activity was higher in all treated groups (35%, 43% and 50%, respectively). After 24 hours, SOD activity was lower (42%) in group 10 mg/kg when compared to control. Groups 10 and 50 mg/kg showed increased GST activity (55% and 43%, respectively). Akt was 48% higher after 50mg/kg dose as compared to control. Besides that acute DHEA administration induced increase in oxidative damage and reduced antioxidant defenses, after 24 h those effects were not seen and a cellular survival pathway was activated. Supported by FAPERGS and CNPq.