Cavernosal tissue nitrite, nitrate, malondialdehyde and glutathione levels in diabetic and non-diabetic erectile dysfunction

Creative Commons License

Tuncayengin A., Biri H., ONARAN M., Sen İ., Tuncayengin O., Polat F., ...More

INTERNATIONAL JOURNAL OF ANDROLOGY, vol.26, no.4, pp.250-254, 2003 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 26 Issue: 4
  • Publication Date: 2003
  • Doi Number: 10.1046/j.1365-2605.2003.00427.x
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.250-254
  • Keywords: diabetes mellitus, erectile dysfunction, glutathione, malondialdehyde, nitric oxide, SMOOTH-MUSCLE RELAXATION, GLYCATION END-PRODUCTS, LIPID-PEROXIDATION, PENILE ERECTION, DEPENDENT INHIBITION, OXIDE, LIVER, RATS, IMPOTENCE, PROTEIN
  • Gazi University Affiliated: Yes


The aim of this study is to investigate the role of nitric oxide (NO) stabile end products, membrane lipid peroxidation and antioxidant defensive mechanism in diabetic erectile dysfunction (ED) and compare these parameters with non-diabetic ED groups. We examined the penile cavernosal tissues, obtained from 22 patients who had undergone surgery of penile prostheses implantation, for the nitrite, nitrate, malondialdehyde (MDA) and glutathione (GSH) levels. Eight patients were suffering from diabetic erectile dysfunction (ED) and 14 patients had non-diabetic ED. Nitrite and nitrate levels were lower; MDA and GSH levels were higher in the diabetic group. There were statistically significant differences between diabetic and non-diabetic groups amongst the nitrite (p < 0.001), nitrate (p < 0.01), MDA (p < 0.001) and GSH (p < 0.01) levels. Our data provide evidence that NO deficiency, possibly due to the membrane lipid peroxidation and defective antioxidant defensive mechanism, may contribute to the development of diabetic ED and thus is involved in the pathogenesis of ED in diabetic patients.