Impairment of male reproductive function after sleep deprivation

Capsule:
Sleep loss can promote marked changes in the male reproductive system in rodents, affecting especially the spermatic function by means of NO pathway modulation.

Authors:
Tathiana A. Alvarenga, Ph.D., Camila Hirotsu, Ph.D., Renata Mazaro-Costa, Ph.D., Sergio Tufik, M.D., Ph.D., Monica L. Andersen, Ph.D.

Volume 103, Issue 5, Pages 1355-1362

Abstract:

Objective:
To evaluate the influence of sleep loss on sexual behavior, hormone levels, sperm parameters, and testis-specific gene expression in male rats.

Design:
Experimental research.

Setting:
Animal laboratory.

Animal(s):
Male adult Wistar-Hannover rats.

Intervention(s):
Sexually experienced rats were subjected to paradoxic sleep deprivation (PSD) for 96 hours or sleep restriction (SR) for 21 days or kept in their home cage as control (CTRL).

Main Outcome Measure(s):
Sexual behavior, hormone levels, sperm parameters and expression of stress and nitric oxide–related genes were evaluated.

Result(s):
PSD significantly decreased sexual behavior compared with the CTRL group, whereas SR had no effect. The PSD group had significantly lower testosterone levels than the CTRL group. Both PSD and SR groups had lower sperm viabilities than the CTRL group. The decrease in the number of live sperm compared with the CTRL group was larger in the PSD group than in the SR group. Regarding testicular gene expression, both PSD and SR led to an increase of iNOS and hydroxysteroid 11β-dehydrogenase 1 expressions compared with the CTRL group. These changes were more pronounced in the PSD group. A significant increase in endothelial nitric oxide synthase expression was observed in the PSD groups compared with the CTRL group. No changes were observed in dimethylarginine dimethylaminohydrolase 1 and casein kinase 2β-polypeptide expressions.

Conclusion(s):
Sleep loss can promote marked changes in the male reproductive system of rats, particularly affecting spermatic function in part by interfering in the testicular nitric oxide pathway.

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