Sildenafil citrate as a phosphodiesterase inhibitor has an antioxidant effect in the blood of men

Summary Background and objective:  Sildenafil citrate enhances the action of nitric oxide by preventing the hydrolysis of cGMP, and is widely used to treat erectile dysfunction. We investigated the effects of sildenafil citrate administration on lipid peroxidation and antioxidant redox enzymes in bl...

Full description

Saved in:
Bibliographic Details
Published inJournal of clinical pharmacy and therapeutics Vol. 33; no. 6; pp. 635 - 640
Main Authors Perk, H., Armagan, A., Nazıroğlu, M., Soyupek, S., Hoscan, M. B., Sütcü, R., Ozorak, A., Delibas, N.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.12.2008
Blackwell
Subjects
Online AccessGet full text
ISSN0269-4727
1365-2710
1365-2710
DOI10.1111/j.1365-2710.2008.00962.x

Cover

Loading…
More Information
Summary:Summary Background and objective:  Sildenafil citrate enhances the action of nitric oxide by preventing the hydrolysis of cGMP, and is widely used to treat erectile dysfunction. We investigated the effects of sildenafil citrate administration on lipid peroxidation and antioxidant redox enzymes in blood of healthy men. Method:  Thirty healthy male subjects were divided equally into two groups. The first group was used as the control. A single dose of sildenafil citrate was administrated orally to subjects constituting the second group. Blood samples were obtained at 0, 2, 6 and 24 h after intake of the single dose of 100 mg sildenafil citrate or placebo. Results and discussion:  The dose of sildenafil citrate resulted in significant increase in the erythrocyte superoxide dismutase and catalase activities at 6 and 24 h. Plasma lipid peroxidation levels decreased slightly. There was no statistical difference in erythrocyte glutathione peroxidase activity between the placebo and sildenafil citrate groups. Conclusion:  Treatment of blood with 100 mg sildenafil citrate has protective effects on oxidative stress by inhibiting free radical formation and by supporting antioxidant redox systems.
Bibliography:ark:/67375/WNG-RFNJ5ZR5-C
istex:01887303B687EF34939C7D76C83CC2758F33A02F
ArticleID:JCPT962
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Undefined-3
ISSN:0269-4727
1365-2710
1365-2710
DOI:10.1111/j.1365-2710.2008.00962.x