H-Index
75
Scimago Lab
powered by Scopus
JCR
Clarivate
Analytics
18%
Acceptance
Rate
call: +1.631.470.9640
Mon-Fri 10 am - 2 pm EST

Logo



eISSN: 1643-3750

Get your full text copy in PDF

Influence of dehydroepiandrosterone on platelet aggregation, superoxide dismutase activity and serum lipid peroxide concentration in rabbits with induced hypercholesterolemia

Grażyna Bednarek-Tupikowska, Izabela Gosk, Andrzej Szuba, Anna Bohdanowicz-Pawlak, Barbara Kosowska, Bożena Bidzińska, Andrzej Milewicz

Med Sci Monit 2000; 6(1): BR40-45

ID: 509259


Special interest in the role of DHEA dates back to the finding of a correlation between low serum DHEA concentrations and a higher morbidity and mortality rate due to coronary diseases in humans. Animal studies with experimental atherosclerosis confirmed the anti-sclerotic effect of DHEA. The mechanism of DHEA action remains unclear. We determined the influence of dehydroepiandrosterone (DHEA) administration, a potential anti-atherogenic agent, on platelet aggregation, platelet superoxide dismutase (SOD) activity and serum lipid peroxide (LPO) levels in male rabbits fed on a normal and atherogenic diet. 44 adult male New Zealand white rabbits were divided into 4 groups: 1 - control group fed on standard rabbit food, 2 - fed on an atherogenic diet, 3 -fed on an atherogenic diet with DHEA, 4 - fed on standard food with DHEA. We detected blood platelet aggregation following (ADP) and collagen activation by means of photometry. Platelet SOD activity was detected by means of fluorometry determining the inhibition of adrenaline auto-oxidation. The serum LPO concentration was measured by means of the colorimetric method. The serum DHEA-S concentration was measured by means of RIA methods, and serum lipid levels were measured by means of Biomérieux manufactured kits. Results demonstrate that (1) elevated LPO concentrations in rabbits with hyperlipidemia did not decrease following DHEA administration. (2) In rabbits fed on a normal diet, DHEA caused a decrease of LPO, which emphasizes the positive influence of this steroid on the oxidative stress in healthy animals. Such a result was not seen in the group with severe hyperlipidemia. (3) Rabbits with hyperlipidemia demonstrated a significantly decreased SOD activity. (4) In healthy animals as well as in those with hyperlipidemia, DHEA administration caused an increase of platelet SOD activity, the main enzyme of the antioxidant defence system, which protects the organism against free radical damage (5) (DHEA had no influence on platelets aggregation in both tested groups). In conclusion: DHEA administration improves platelet SOD activity, which protects cells against oxidative damage. The hypothesis that DHEA administration leads to an increase in antioxidant potency requires further investigations.

This paper has been published under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.
I agree