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

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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.

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Most cited references 26

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Antioxidant therapies in traumatic brain and spinal cord injury.

Mona Bains, Edward Hall (2012)

Free radical formation and oxidative damage have been extensively investigated and validated as important contributors to the pathophysiology of acute central nervous system injury. The generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) is an early event following injury occurring within minutes of mechanical impact. A key component in this event is peroxynitrite-induced lipid peroxidation. As discussed in this review, peroxynitrite formation and lipid peroxidation irreversibly damages neuronal membrane lipids and protein function, which results in subsequent disruptions in ion homeostasis, glutamate-mediated excitotoxicity, mitochondrial respiratory failure and microvascular damage. Antioxidant approaches include the inhibition and/or scavenging of superoxide, peroxynitrite, or carbonyl compounds, the inhibition of lipid peroxidation and the targeting of the endogenous antioxidant defense system. This review covers the preclinical and clinical literature supporting the role of ROS and RNS and their derived oxygen free radicals in the secondary injury response following acute traumatic brain injury (TBI) and spinal cord injury (SCI) and reviews the past and current trends in the development of antioxidant therapeutic strategies. Combinatorial treatment with the suggested mechanistically complementary antioxidants will also be discussed as a promising neuroprotective approach in TBI and SCI therapeutic research. This article is part of a Special Issue entitled: Antioxidants and antioxidant treatment in disease. Copyright Â© 2011 Elsevier B.V. All rights reserved.

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Testosterone and oxidative stress: the oxidation handicap hypothesis.

Olivier Chastel, Gabriele Sorci, Sophie Bertrand … (2007)

Secondary sexual traits (SST) are usually thought to have evolved as honest signals of individual quality during mate choice. Honesty of SST is guaranteed by the cost of producing/maintaining them. In males, the expression of many SST is testosterone-dependent. The immunocompetence handicap hypothesis has been proposed as a possible mechanism ensuring honesty of SST on the basis that testosterone, in addition to its effect on sexual signals, also has an immunosuppressive effect. The immunocompetence handicap hypothesis has received mixed support. However, the cost of testosterone-based signalling is not limited to immunosuppression and might involve other physiological functions such as the antioxidant machinery. Here, we tested the hypothesis that testosterone depresses resistance to oxidative stress in a species with a testosterone-dependent sexual signal, the zebra finch. Male zebra finches received subcutaneous implants filled with flutamide (an anti-androgen) or testosterone, or kept empty (control). In agreement with the prediction, we found that red blood cell resistance to a free radical attack was the highest in males implanted with flutamide and the lowest in males implanted with testosterone. We also found that cell-mediated immune response was depressed in testosterone-treated birds, supporting the immunocompetence handicap hypothesis. The recent finding that red blood cell resistance to free radicals is negatively associated with mortality in this species suggests that benefits of sexual signalling might trade against the costs derived from oxidation.

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Testosterone influences basal metabolic rate in male house sparrows: a new cost of dominance signalling?

K Buchanan, M. R. Evans, A Goldsmith … (2001)

Sexually selected signals of individual dominance have profound effects on access to resources, mate choice and gene flow. However, why such signals should honestly reflect individual quality is poorly understood. Many such signals are known to develop under the influence of testosterone. We conducted an experiment in male house sparrows in which testosterone was manipulated independently during two periods: before the onset of the breeding season and prior to the autumn moult. We then measured the effects of these manipulations on basal metabolic rate and on the size of the chest bib, a sexually selected signal. The results demonstrate that testosterone simultaneously affects both signal development and basal metabolic rate in the house sparrow (Passer domesticus). This evidence, therefore, supports a novel conclusion: that testosterone-dependent signals act as honest indicators of male quality possibly because only high-quality individuals can sustain the energetic costs associated with signal development.

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Author and article information

Journal

Journal ID (nlm-ta): Int J Fertil Steril

Journal ID (iso-abbrev): Int J Fertil Steril

Journal ID (publisher-id): Royan Institute

Title: International Journal of Fertility & Sterility

Publisher: Royan Institute

ISSN (Print): 2008-076X

ISSN (Electronic): 2008-0778

Publication date (Print): Apr-Jun 2016

Publication date (Electronic): 5 April 2016

Volume: 10

Issue: 1

Pages: 87-93

Affiliations

[1 ]Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

[2 ]School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran

[3 ]Zoonosis Research Center, Tehran University of Medical Sciences, Tehran, Iran

[4 ]Department of Urology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

[5 ]Department of Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

[6 ]Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

[7 ]Department of Anatomy, School of Medicine, Kermanshah University of Medical Science, Kermanshah, Iran

Author notes

[*Corresponding Address: ]P.O.Box: 6447-14155Department of AnatomySchool of MedicineTehran University of Medical Sciences TehranIran Email: hassanzadeh@ 123456tums.ac.ir

Article

Other ID: Int-J-Fertil-Steril-10-87

PMC ID: 4845534

PubMed ID: 27123205

SO-VID: 316d0d42-bd28-4edc-b57b-7e1ece9c4099

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 2 December 2013

Date accepted : 24 May 2015

Custom metadata

Citation Choobineh H, Sadighi Gilani MA, Pasalar P, Jahanzad I, Ghorbani R, Hassanzadeh G. The effects of testos- terone on oxidative stress markers in mice with spinal cord injuries. Int J Fertil Steril. 2016; 10(1): 87-93.

Keywords: spinal cord injury,infertility,testosterone,oxidative stress,reactive oxygen species

Data availability:

Keywords: spinal cord injury, infertility, testosterone, oxidative stress, reactive oxygen species

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

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Abstract

Background

Materials and Methods

Results

Conclusion

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Stress signalling in stem cells

Most cited references 26

Antioxidant therapies in traumatic brain and spinal cord injury.

Testosterone and oxidative stress: the oxidation handicap hypothesis.

Testosterone influences basal metabolic rate in male house sparrows: a new cost of dominance signalling?

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