Alteration Expression of Bax, Bcl-2 and VDAC1 Genes in Oligozoospermic and Fertile Subjects
Author(s) -
Arni Amir,
Yanwirasti Yanwirasti,
Asmarinah Asmarinah,
Fadil Oenzil
Publication year - 2016
Publication title -
pakistan journal of biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.268
H-Index - 43
eISSN - 1812-5735
pISSN - 1028-8880
DOI - 10.3923/pjbs.2016.71.76
Subject(s) - vdac1 , biology , complementary dna , gene , microbiology and biotechnology , apoptosis , voltage dependent anion channel , spermatogenesis , gene expression , andrology , genetics , bacterial outer membrane , endocrinology , medicine , escherichia coli
One of factors causing oligozoospermic circumstances is excessive apoptosis during spermatogenesis. Spermatogenesis known involves Bcl-2 family proteins in cytoplasm and Voltage Dependent Anion Channel 1 (VDAC1) in outer mitochondrial membrane to facilitate releasing of apoptosis factor such as cytochrome-c from inter-membrane space into cytoplasm. The study was aimed to analyze the mRNA expression of pro-apoptotic Bax, anti-apoptotic Bcl-2 and VDAC1 genes derived from 45 oligozoospermic subjects and 20 fertile subjects as control. Analysis of transcript expression was performed by two-steps real-time (PCR) and calculating by standard curve method. Stages of works were followed: Analysis of sperm basal characterization, isolation of spermatozoa to separate it from cement and resulted pellets. Pellets were saturated with PBS to obtain mRNA and reversed into cDNA. The cDNA were sequenced to investigate SNP of Bax, Bcl-2 and VDAC1 genes. Results showed that comparison of log mRNA copy number of Bax, Bcl-2 and VDAC1 genes for oligospemic and fertile subjects varied. The Bax, Bcl-2 and VDAC1 were significantly different between oligozoospermic and normozoospermic subjects (p = 0.000, p = 0.041, p = 0.000, respectively). It was suggested that oligozoospermia may be occurred by inducing the increase of Bax pro-apoptotic and VDAC1 genes expression and decreasing of Bcl-2 expression to lead the excessive of apoptosis.
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