The expression of Bax protein in the early stages of spinal cord injury in the sperm cells of rats
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Department of Anatomy and Neuroscience, Shahrekord University of Medical Sciences, Shahrekord, Iran
Department of Surgery, Faculty of Medicine, Kurdistan University of Medical Sciences, Kurdistan, Iran
Department of Anatomy and Reproductive Biology, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran
Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Lorestan University of Medical Sciences, Khorramabad, Iran
Deputy of Research, Kurdistan University of Medical Sciences, Sanandaj, Iran
Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran
Mohammad Jafar Rezaie   

Cellular and Molecular Research Center, Department of Anatomical Sciences, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran. Tel.: +988733664653, Fax: +988716664663.
Submission date: 2017-04-19
Acceptance date: 2017-07-11
Online publication date: 2018-06-18
Publication date: 2019-11-18
Pol. Ann. Med. 2018;25(2):196–202
Apoptosis is one of the most important biological processes, which occurs through the activation of intracellular cell death pathway.

The aim of this study was to determine the pattern of cell death within the early stages of spinal cord injury (SCI) and the evaluation of the changes in Bax protein expression of progressive apoptosis.

Material and methods:
48 adult male Sprague Dawley rats were randomly divided into two control and experimental groups. Animals were anesthetized and then the laminectomy procedure was performed in the area of T6–8. On days 1, 7, 14 and 28 after the surgery, one-third of the middle part of their testis tissue were taken for histological and immunohistochemical analysis.

The immunohistochemical analysis indicated the presence of TUNEL-positive cells and cells containing the pro-apoptotic protein Bax in testicular sperms in the 1st day after SCI, as well as increased on 28 days.

1 day after SCI, the apoptosis occurred in testicular sperm lines as well as the apoptosis can be related to Bax protein expression. Therefore inhibition of caspase activity via caspase cascades-mediated apoptosis may have a protective role in testicular injury during the acute phase of SCI.

Our finding suggested that the damage and destruction after SCI can be controlled by therapeutic interventions at the appropriate time before the destructive changes of SCI.

Authors would like to thank personnel of deputy of research and lab staffs in Kurdistan University of Medical Sciences, Sanandaj, Iran for their technical and assistant support.
The authors declare no conflict of interest.
Wyndaele M, Wyndaele J-J. Incidence, prevalence and epidemiology of spinal cord injury: what learns a worldwide literature survey? Spinal Cord. 2006;44(9):523–529.
Beattie MS, Hermann GE, Rogers RC, Bresnahan JC. Cell death in models of spinal cord injury. Prog Brain Res. 2002;137:37–47.
Shimada K, Crother TR, Karlin J, et al. Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. Immunity. 2012;36(3):401–414.
Caruso RA, Fedele F, Rigoli L, et al. Apoptotic-like tumor cells and apoptotic neutrophils in mitochondrion-rich gastric adenocarcinomas: a comparative study with light and electron microscopy between these two forms of cell death. Rare Tumors. 2013;5(2):68–71.
Xie Y, Li Q, Yang Q, et al. Overexpression of DCF1 inhibits glioma through destruction of mitochondria and activation of apoptosis pathway. Scientific Rep. 2014;4:3702.
Burda JE, Sofroniew MV. Reactive gliosis and the multicellular response to CNS damage and disease. Neuron. 2014;81(2):229–248.
Wang Y, Sun Z, Zhang K, Xu G, Li G. Bcl-2 in suppressing neuronal apoptosis after spinal cord injury. World J Emerg Med. 2011;2(1):38–44.
Levkovitch-Verbin H, Waserzoog Y, Vander S, Makarovsky D, Ilia P. Minocycline mechanism of neuroprotection involves the Bcl-2 gene family in optic nerve transection. Int J Neurosci. 2014;124(10):755–761.
Ashkenazi A, Salvesen G. Regulated cell death: signaling and mechanisms. Annu Rev Cell Dev Biol. 2014;30:337–356.
Tiraihi T, Rezaie MJ. Apoptosis onset and Bax protein distribution in spinal motoneurons of newborn rats following sciatic nerve axotomy. Int J Neurosci. 2003;113(9):1163–1175.
Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol. 2007;35(4):495–516.
Snigdha S, Smith ED, Prieto GA, Cotman CW. Caspase-3 activation as a bifurcation point between plasticity and cell death. Neurosci Bull. 2012;28(1):14–24.
Miranpuri GS, Meethal SV, Sampene E, et al. Folic Acid Modulates Matrix Metalloproteinase-2 Expression, Alleviates Neuropathic Pain, and Improves Functional Recovery in Spinal Cord-Injured Rats. Ann Neurosci. 2017;24:74–81.
Cramer SW, Baggott C, Cain J, et al. The role of cation-dependent chloride transporters in neuropathic pain following spinal cord injury. Mol Pain. 2008;4:36.
Basso DM, Beattie MS, Bresnahan JC. A sensitive and reliable locomotor rating scale for open field testing in rats. J Neurotrauma. 1995;12(1):1–21.
National Research Council. Committee for the Update of the Guide for the Care and Use of Laboratory Animals. Guide for the Care and Use of Laboratory Animals. Eight Edition. Washington: The National Academiess Press. 2011. Accessed June 5, 2018.
Poon PC, Gupta D, Shoichet MS, Tator CH. Clip compression model is useful for thoracic spinal cord injuries: histologic and functional correlates. Spine. 2007;32(25):2853–2859.
Johnsen SG. Testicular biopsy score count–a method for registration of spermatogenesis in human testes: normal values and results in 335 hypogonadal males. Hormones. 1970;1(1):2–25.
Nasimi P, Vahdati A, Tabandeh M, Khatamsaz S. Cytoprotective and anti-apoptotic effects of Satureja khuzestanica essential oil against busulfan-mediated sperm damage and seminiferous tubules destruction in adult male mice. Andrologia. 2016;48(1):74–81.
Knudson CM, Tung KS, Tourtellotte WG, Brown GA, Korsmeyer SJ. Bax-deficient mice with lymphoid hyperplasia and male germ cell death. Science. 1995;270(5233):96–99.
Hirsch IH, Huang B, Chancellor MB, et al. Spermatogenesis in early and chronic phases of experimental spinal cord injury in the rodent model. J Androl. 1999;20(1):63–71.
Chow S-H, Giglio W, Anesetti R, Ottenweller JE, Pogach LM, Huang HF. The effects of testicular denervation on spermatogenesis in the Sprague-Dawley rat. Neuroendocrinology. 2000;72(1):37–45.
Patki P, Woodhouse J, Hamid R, Craggs M, Shah J. Effects of spinal cord injury on semen parameters. J Spinal Cord Med. 2008;31(1):27–32.
Ohl DA, Sønksen J, Wedemeyer G, et al. Canine model of infertility after spinal cord injury: time course of acute changes in semen quality and spermatogenesis. J Urol. 2001;166(3):1181–1184.
Muriel L, Goyanes V, Segrelles E, Gosálvez J, Alvarez JG, Fernández JL. Increased aneuploidy rate in sperm with fragmented DNA as determined by the sperm chromatin dispersion (SCD) test and FISH analysis. J Androl. 2007;28(1):38–49.
Chohan KR, Griffin JT, Lafromboise M, Jonge CJ, Carrell DT. Comparison of chromatin assays for DNA fragmentation evaluation in human sperm. J Androl. 2006;27(1):53–59.
Billups K, Tillman S, Chang T. Reduction of epididymal sperm motility after ablation of the inferior mesenteric plexus in the rat. Fertil Steril. 1990;53(6):1076–1082.