Past Issue

Volume 10, Number 1, Apr-Jun 2016, Pages: 87-93

The Effects of Testosterone on Oxidative Stress Markers in Mice with Spinal Cord Injuries


Hamid Choobineh, M.P.H, Ph.D., 1, 2, 3, Mohammad Ali Sadighi Gilani, M.D, 4, Parvin Pasalar, Ph.D, 5, Issa Jahanzad, Ph.D, 6, Rostam Ghorbani, Ph.D, 7, Gholamreza Hassanzadeh, Ph.D, 1, *,
Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran
Zoonosis Research Center, Tehran University of Medical Sciences, Tehran, Iran
Department of Urology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Department of Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Department of Anatomy, School of Medicine, Kermanshah University of Medical Science, Kermanshah, Iran
*Corresponding Address: P.O.Box: 6447-14155 Department of Anatomy School of Medicine Tehran University of Medical Sciences Tehran Iran Email:hassanzadeh@tums.ac.ir

Abstract

Background

Spinal cord injury (SCI) causes infertility in male patients through erectile dysfunction, ejaculatory dysfunction, semen and hormone abnormalities. Oxidative stress (OS) is involved in poor semen quality and subsequent infertility in males with SCI. The aim of this study is to examine the effects of SCI on the level of testosterone hormone.

Materials and Methods

In this experimental study, we evaluated the effects of exogenous testosterone on the activity of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx) as well as the levels of malondialdehyde (MDA) and protein carbonylation (PCO), as markers of OS, in 10 groups of SCI mice. Total antioxidant capacity (TAC) was determined using the 2,29-azinobis-(3-ethylbenzothiazoline- 6-sulfonic acid) (ABTS) radical cation assay.

Results

Exogenous testosterone administration in mice with SCI significantly reduced SOD and GPx enzyme activities and MDA level. There was no significant decrease in PCO content. In addition, TAC remarkably increased in the sham and SCI groups not treated with testosterone but remained unchanged in all other experimental groups. Exogenous testosterone also reduced serum testosterone levels in all groups except the positive control group.

Conclusion

Our cumulative data indicated that SCI could cause sterility by disturbing the plasmatic testosterone balance. The normal level of endogenous testosterone was not completely restored by exogenous testosterone administration.