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Transnitrosylation: A Factor in Nitric Oxide-Mediated Penile Erection
Biljana Musicki1, Gwen Lagoda1, Tabitha Goetz1
1The James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
The Journal of Sexual Medicine
|April 27, 2016
Summary
S-nitrosoglutathione reductase (GSNOR) deficiency impairs erectile function by disrupting endothelial nitric oxide synthase (eNOS) activity and increasing oxidative stress in the penis.
Area of Science:
- Physiology
- Biochemistry
- Urology
Background:
- Nitric oxide (NO) mediates signaling via cyclic guanosine monophosphate and S-nitrosylation.
- The role of S-nitrosylation in erectile function, NO regulation, and penile oxidative stress is not well understood.
Purpose of the Study:
- To investigate the function of S-nitrosoglutathione reductase (GSNOR) in regulating erectile function.
- To determine GSNOR's impact on endothelial NO synthase (eNOS) activity and oxidative stress in the penis.
Main Methods:
- Adult GSNOR-deficient and wild-type mice were used.
- Erectile function was assessed via cavernous nerve stimulation.
- Penile S-nitrosylation, eNOS phosphorylation, uncoupling, and oxidative stress markers were measured.
Main Results:
- GSNOR deficiency did not affect baseline erectile function but impaired eNOS activation upon stimulation.
- Total S-nitrosylated proteins increased in GSNOR-deficient mice.
- Penile NO production decreased, while eNOS uncoupling and oxidative stress markers (4-HNE, MDA, nitrotyrosine) increased.
Conclusions:
- Transnitrosylation is crucial for regulating penile NO bioactivity.
- GSNOR deficiency leads to eNOS dysfunction and heightened oxidative damage, indicating its role in maintaining penile homeostasis.
Keywords:
Endothelial Nitric Oxide SynthaseEndothelial Nitric Oxide Synthase UncouplingErectile FunctionMouseOxidative-Nitrosative StressS-Nitrosoglutathione ReductaseS-NitrosylationMore Related Videos
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