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The Effects of Testosterone on Oxidative Stress Markers in Mice with Spinal Cord Injuries
Hamid Choobineh1, Mohammad Ali Sadighi Gilani2, Parvin Pasalar3
1Department 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.
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.
Insights
Spinal cord injury (SCI) disrupts male testosterone balance, leading to infertility. Exogenous testosterone did not fully restore normal hormone levels in SCI mice, indicating complex hormonal disturbances.
Area of Science:
- Reproductive Endocrinology
- Neuroscience
- Biochemistry
Background:
- Spinal cord injury (SCI) frequently results in male infertility due to erectile dysfunction, ejaculatory issues, and hormonal imbalances.
- Oxidative stress (OS) is a significant contributor to poor semen quality and infertility in males affected by SCI.
- Understanding the impact of SCI on testosterone levels is crucial for addressing male infertility.
Purpose of the Study:
- To investigate the effects of spinal cord injury (SCI) on circulating testosterone levels in a mouse model.
- To evaluate the influence of exogenous testosterone administration on oxidative stress markers and antioxidant enzyme activity in SCI mice.
Main Methods:
- Experimental study involving 10 groups of SCI mice to assess the impact of exogenous testosterone.
- Measurement of antioxidant enzymes (superoxide dismutase, glutathione peroxidase) and oxidative stress markers (malondialdehyde, protein carbonylation).
- Determination of total antioxidant capacity (TAC) using the ABTS radical cation assay.
Main Results:
- Exogenous testosterone administration significantly decreased superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and malondialdehyde (MDA) levels in SCI mice.
- Protein carbonylation (PCO) levels did not show a significant decrease.
- Total antioxidant capacity (TAC) increased in sham and untreated SCI groups but remained unchanged with testosterone treatment; serum testosterone levels decreased in most treated groups.
Conclusions:
- Spinal cord injury (SCI) disrupts plasmatic testosterone balance, potentially causing sterility in males.
- Exogenous testosterone administration did not fully restore endogenous testosterone levels in SCI mice.
- The study highlights the complex interplay between SCI, oxidative stress, and hormonal regulation in male infertility.
