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DOI 10.22074/cellj.2018.5003

Медицинская библиотека · Cell journal · 2018

Testosterone Reduces Spinal Cord Injury-Induced Effects on Male Reproduction by Preventing CADM1 Defect.

Choobineh Hamid, Kazemi Mahsa, Sadighi Gilani Mohammad Ali, Heydari Tahereh, Shokri Saeed, Bazrafkan Mahshid, Hassanzadeh Gholamreza

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Аннотация

OBJECTIVES

This study evaluated the effects of exogenous testosterone molecule-1 (CADM1) pathological defect during early and chronic periods of spinal cord injury (SCI).

MATERIALS AND

METHODS

In this experimental study, Testosterone was administered immediately or after one week of SCI induction. Along with quantification of CADM1 gene expression and its immunoreactivity, we evaluated sperm parameters and serum testosterone level post-SCI.

RESULTS

Different grades of abnormalities in sperm parameters and testis architecture were observed along with significant reductions in the level of CADM1 expression and its immunoreactivity in the seminiferous tubules of both acute and chronic SCI groups. Exogenous testosterone, by compensating the serum testosterone level. reduced the percentage of apoptotic and both short head and abnormal sperm froms in the caudal epididymis. Importantly, the beneficial effects of immediate administration of testosterone were prominent. Increases in the level of CADM1 transcription and its immunoreactivity in the testis of SCI mice treated with testosterone were accompanied by improvement of sperm motility as well as testicular Johnsen's and Miller's criteria.

CONCLUSIONS

Since immediate testosterone treatment improved the immunoreactivity and transcription level of CADM1, the observed beneficial effect of exogenouse testosterone can be attributed to its effect on CADM1 dynamics.

Для цитирования: Choobineh Hamid, Kazemi Mahsa, Sadighi Gilani Mohammad Ali, Heydari Tahereh, Shokri Saeed, Bazrafkan Mahshid, Hassanzadeh Gholamreza. Testosterone Reduces Spinal Cord Injury-Induced Effects on Male Reproduction by Preventing CADM1 Defect.. Cell journal. 2018. DOI: 10.22074/cellj.2018.5003.
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